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Current Medicinal Chemistry

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ISSN (Online): 1875-533X

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Review Article

Biological Consequences of Dysfunctional HDL

Author(s): Angela Pirillo *, Alberico Luigi Catapano* and Giuseppe Danilo Norata

Volume 26, Issue 9, 2019

Page: [1644 - 1664] Pages: 21

DOI: 10.2174/0929867325666180530110543

Price: $65

Abstract

Epidemiological studies have suggested an inverse correlation between high-density lipoprotein (HDL) cholesterol levels and the risk of cardiovascular disease. HDLs promote reverse cholesterol transport (RCT) and possess several putative atheroprotective functions, associated to the anti-inflammatory, anti-thrombotic and anti-oxidant properties as well as to the ability to support endothelial physiology.

The assumption that increasing HDL-C levels would be beneficial on cardiovascular disease (CVD), however, has been questioned as, in most clinical trials, HDL-C-raising therapies did not result in improved cardiovascular outcomes. These findings, together with the observations from Mendelian randomization studies showing that polymorphisms mainly or solely associated with increased HDL-C levels did not decrease the risk of myocardial infarction, shift the focus from HDL-C levels toward HDL functional properties. Indeed, HDL from atherosclerotic patients not only exhibit impaired atheroprotective functions but also acquire pro-atherogenic properties and are referred to as “dysfunctional” HDL; this occurs even in the presence of normal or elevated HDL-C levels. Pharmacological approaches aimed at restoring HDL functions may therefore impact more significantly on CVD outcome than drugs used so far to increase HDL-C levels. The aim of this review is to discuss the pathological conditions leading to the formation of dysfunctional HDL and their role in atherosclerosis and beyond.

Keywords: High density lipoprotein, dysfunctional HDL, HDL quality, HDL subfractions, atherosclerosis, cardiovascular disease, epidemiological studies, apolipoprotein-A.

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[1]
Di Angelantonio, E.; Sarwar, N.; Perry, P.; Kaptoge, S.; Ray, K.K.; Thompson, A.; Wood, A.M.; Lewington, S.; Sattar, N.; Packard, C.J.; Collins, R.; Thompson, S.G.; Danesh, J. Major lipids, apolipoproteins, and risk of vascular disease. JAMA, 2009, 302(18), 1993-2000.
[2]
Kontush, A. HDL-mediated mechanisms of protection in cardiovascular disease. Cardiovasc. Res., 2014, 103(3), 341-349.
[3]
Remaley, A.T.; Norata, G.D.; Catapano, A.L. Novel concepts in HDL pharmacology. Cardiovasc. Res., 2014, 103(3), 423-428.
[4]
Parolini, C.; Marchesi, M.; Lorenzon, P.; Castano, M.; Balconi, E.; Miragoli, L.; Chaabane, L.; Morisetti, A.; Lorusso, V.; Martin, B.J.; Bisgaier, C.L.; Krause, B.; Newton, R.S.; Sirtori, C.R.; Chiesa, G. Dose-related effects of repeated ETC-216 (recombinant apolipoprotein A-I Milano/1-palmitoyl-2-oleoyl phosphatidylcholine complexes) administrations on rabbit lipid-rich soft plaques: in vivo assessment by intravascular ultrasound and magnetic resonance imaging. J. Am. Coll. Cardiol., 2008, 51(11), 1098-1103.
[5]
Ibanez, B.; Vilahur, G.; Cimmino, G.; Speidl, W.S.; Pinero, A.; Choi, B.G.; Zafar, M.U.; Santos-Gallego, C.G.; Krause, B.; Badimon, L.; Fuster, V.; Badimon, J.J. Rapid change in plaque size, composition, and molecular footprint after recombinant apolipoprotein A-I Milano (ETC-216) administration: magnetic resonance imaging study in an experimental model of atherosclerosis. J. Am. Coll. Cardiol., 2008, 51(11), 1104-1109.
[6]
Giannarelli, C.; Cimmino, G.; Ibanez, B.; Chiesa, G.; Garcia-Prieto, J.; Santos-Gallego, C.G.; Alique-Aguilar, M.; Fuster, V.; Sirtori, C.; Badimon, J.J. Acute ApoA-I Milano administration induces plaque regression and stabilisation in the long term. Thromb. Haemost., 2012, 108(6), 1246-1248.
[7]
Nissen, S.E.; Tsunoda, T.; Tuzcu, E.M.; Schoenhagen, P.; Cooper, C.J.; Yasin, M.; Eaton, G.M.; Lauer, M.A.; Sheldon, W.S.; Grines, C.L.; Halpern, S.; Crowe, T.; Blankenship, J.C.; Kerensky, R. Effect of recombinant ApoA-I Milano on coronary atherosclerosis in patients with acute coronary syndromes: a randomized controlled trial. JAMA, 2003, 290(17), 2292-2300.
[8]
Tardif, J.C.; Grégoire, J.; L’Allier, P.L.; Ibrahim, R.; Lespérance, J.; Heinonen, T.M.; Kouz, S.; Berry, C.; Basser, R.; Lavoie, M.A.; Guertin, M.C.; Rodés-Cabau, J. Effects of reconstituted high-density lipoprotein infusions on coronary atherosclerosis: a randomized controlled trial. JAMA, 2007, 297(15), 1675-1682.
[9]
Shaw, J.A.; Bobik, A.; Murphy, A.; Kanellakis, P.; Blombery, P.; Mukhamedova, N.; Woollard, K.; Lyon, S.; Sviridov, D.; Dart, A.M. Infusion of reconstituted high-density lipoprotein leads to acute changes in human atherosclerotic plaque. Circ. Res., 2008, 103(10), 1084-1091.
[10]
Nicholls, S.J.; Tuzcu, E.M.; Sipahi, I.; Schoenhagen, P.; Crowe, T.; Kapadia, S.; Nissen, S.E. Relationship between atheroma regression and change in lumen size after infusion of apolipoprotein A-I Milano. J. Am. Coll. Cardiol., 2006, 47(5), 992-997.
[11]
Boden, W.E.; Probstfield, J.L.; Anderson, T.; Chaitman, B.R.; Desvignes-Nickens, P.; Koprowicz, K.; McBride, R.; Teo, K.; Weintraub, W. Niacin in patients with low HDL cholesterol levels receiving intensive statin therapy. N. Engl. J. Med., 2011, 365(24), 2255-2267.
[12]
Schwartz, G.G.; Olsson, A.G.; Abt, M.; Ballantyne, C.M.; Barter, P.J.; Brumm, J.; Chaitman, B.R.; Holme, I.M.; Kallend, D.; Leiter, L.A.; Leitersdorf, E.; McMurray, J.J.; Mundl, H.; Nicholls, S.J.; Shah, P.K.; Tardif, J.C.; Wright, R.S. Effects of dalcetrapib in patients with a recent acute coronary syndrome. N. Engl. J. Med., 2012, 367(22), 2089-2099.
[13]
Lincoff, A.M.; Nicholls, S.J.; Riesmeyer, J.S.; Barter, P.J.; Brewer, H.B.; Fox, K.A.A.; Gibson, C.M.; Granger, C.; Menon, V.; Montalescot, G.; Rader, D.; Tall, A.R.; McErlean, E.; Wolski, K.; Ruotolo, G.; Vangerow, B.; Weerakkody, G.; Goodman, S.G.; Conde, D.; McGuire, D.K.; Nicolau, J.C.; Leiva-Pons, J.L.; Pesant, Y.; Li, W.; Kandath, D.; Kouz, S.; Tahirkheli, N.; Mason, D.; Nissen, S.E.; Investigators, A. Evacetrapib and cardiovascular outcomes in high-risk vascular disease. N. Engl. J. Med., 2017, 376(20), 1933-1942.
[14]
Bowman, L.; Hopewell, J.C.; Chen, F.; Wallendszus, K.; Stevens, W.; Collins, R.; Wiviott, S.D.; Cannon, C.P.; Braunwald, E.; Sammons, E.; Landray, M.J. Effects of anacetrapib in patients with atherosclerotic vascular disease. N. Engl. J. Med., 2017, 377(13), 1217-1227.
[15]
Voight, B.F.; Peloso, G.M.; Orho-Melander, M.; Frikke-Schmidt, R.; Barbalic, M.; Jensen, M.K.; Hindy, G.; Hólm, H.; Ding, E.L.; Johnson, T.; Schunkert, H.; Samani, N.J.; Clarke, R.; Hopewell, J.C.; Thompson, J.F.; Li, M.; Thorleifsson, G.; Newton-Cheh, C.; Musunuru, K.; Pirruccello, J.P.; Saleheen, D.; Chen, L.; Stewart, A.; Schillert, A.; Thorsteinsdottir, U.; Thorgeirsson, G.; Anand, S.; Engert, J.C.; Morgan, T.; Spertus, J.; Stoll, M.; Berger, K.; Martinelli, N.; Girelli, D.; McKeown, P.P.; Patterson, C.C.; Epstein, S.E.; Devaney, J.; Burnett, M.S.; Mooser, V.; Ripatti, S.; Surakka, I.; Nieminen, M.S.; Sinisalo, J.; Lokki, M.L.; Perola, M.; Havulinna, A.; de Faire, U.; Gigante, B.; Ingelsson, E.; Zeller, T.; Wild, P.; de Bakker, P.I.; Klungel, O.H.; Maitland-van der Zee, A.H.; Peters, B.J.; de Boer, A.; Grobbee, D.E.; Kamphuisen, P.W.; Deneer, V.H.; Elbers, C.C.; Onland-Moret, N.C.; Hofker, M.H.; Wijmenga, C.; Verschuren, W.M.; Boer, J.M.; van der Schouw, Y.T.; Rasheed, A.; Frossard, P.; Demissie, S.; Willer, C.; Do, R.; Ordovas, J.M.; Abecasis, G.R.; Boehnke, M.; Mohlke, K.L.; Daly, M.J.; Guiducci, C.; Burtt, N.P.; Surti, A.; Gonzalez, E.; Purcell, S.; Gabriel, S.; Marrugat, J.; Peden, J.; Erdmann, J.; Diemert, P.; Willenborg, C.; König, I.R.; Fischer, M.; Hengstenberg, C.; Ziegler, A.; Buysschaert, I.; Lambrechts, D.; Van de Werf, F.; Fox, K.A.; El Mokhtari, N.E.; Rubin, D.; Schrezenmeir, J.; Schreiber, S.; Schäfer, A.; Danesh, J.; Blankenberg, S.; Roberts, R.; McPherson, R.; Watkins, H.; Hall, A.S.; Overvad, K.; Rimm, E.; Boerwinkle, E.; Tybjaerg-Hansen, A.; Cupples, L.A.; Reilly, M.P.; Melander, O.; Mannucci, P.M.; Ardissino, D.; Siscovick, D.; Elosua, R.; Stefansson, K.; O’Donnell, C.J.; Salomaa, V.; Rader, D.J.; Peltonen, L.; Schwartz, S.M.; Altshuler, D.; Kathiresan, S. Plasma HDL cholesterol and risk of myocardial infarction: a mendelian randomisation study. Lancet, 2012, 380(9841), 572-580.
[16]
Silbernagel, G.; Schöttker, B.; Appelbaum, S.; Scharnagl, H.; Kleber, M.E.; Grammer, T.B.; Ritsch, A.; Mons, U.; Holleczek, B.; Goliasch, G.; Niessner, A.; Boehm, B.O.; Schnabel, R.B.; Brenner, H.; Blankenberg, S.; Landmesser, U.; März, W. High-density lipoprotein cholesterol, coronary artery disease, and cardiovascular mortality. Eur. Heart J., 2013, 34(46), 3563-3571.
[17]
März, W.; Kleber, M.E.; Scharnagl, H.; Speer, T.; Zewinger, S.; Ritsch, A.; Parhofer, K.G.; von Eckardstein, A.; Landmesser, U.; Laufs, U. HDL cholesterol: reappraisal of its clinical relevance. Clin. Res. Cardiol., 2017, 106(9), 663-675.
[18]
Pirillo, A.; Norata, G.D.; Catapano, A.L. Treating high density lipoprotein cholesterol (HDL-C): quantity versus quality. Curr. Pharm. Des., 2013, 19(21), 3841-3857.
[19]
Pirillo, A.; Tibolla, G.; Norata, G.D.; Catapano, A.L. HDL: to treat or not to treat? Curr. Atheroscler. Rep., 2014, 16(8), 429.
[20]
Pirillo, A.; Norata, G.D.; Catapano, A.L. High-density lipoprotein subfractions--what the clinicians need to know. Cardiol., 2013, 124(2), 116-125.
[21]
Ossoli, A.; Pavanello, C.; Calabresi, L. High-density lipoprotein, lecithin: cholesterol acyltransferase, and atherosclerosis. Endocrinol. Metab., 2016, 31(2), 223-229.
[22]
Rohatgi, A.; Khera, A.; Berry, J.D.; Givens, E.G.; Ayers, C.R.; Wedin, K.E.; Neeland, I.J.; Yuhanna, I.S.; Rader, D.R.; de Lemos, J.A.; Shaul, P.W. HDL cholesterol efflux capacity and incident cardiovascular events. N. Engl. J. Med., 2014, 371(25), 2383-2393.
[23]
Khera, A.V.; Cuchel, M.; de la Llera-Moya, M.; Rodrigues, A.; Burke, M.F.; Jafri, K.; French, B.C.; Phillips, J.A.; Mucksavage, M.L.; Wilensky, R.L.; Mohler, E.R.; Rothblat, G.H.; Rader, D.J. Cholesterol efflux capacity, high-density lipoprotein function, and atherosclerosis. N. Engl. J. Med., 2011, 364(2), 127-135.
[24]
Saleheen, D.; Scott, R.; Javad, S.; Zhao, W.; Rodrigues, A.; Picataggi, A.; Lukmanova, D.; Mucksavage, M.L.; Luben, R.; Billheimer, J.; Kastelein, J.J.; Boekholdt, S.M.; Khaw, K.T.; Wareham, N.; Rader, D.J. Association of HDL cholesterol efflux capacity with incident coronary heart disease events: a prospective case-control study. Lancet Diabetes Endocrinol., 2015, 3(7), 507-513.
[25]
Ritsch, A.; Scharnagl, H.; März, W. HDL cholesterol efflux capacity and cardiovascular events. N. Engl. J. Med., 2015, 372(19), 1870-1871.
[26]
Millar, J.S.; Cuchel, M. ApoA-I-Directed Therapies for the management of atherosclerosis. Curr. Atheroscler. Rep., 2015, 17(10), 60.
[27]
Dunbar, R.L.; Movva, R.; Bloedon, L.T.; Duffy, D.; Norris, R.B.; Navab, M.; Fogelman, A.M.; Rader, D.J. Oral apolipoprotein A-I mimetic D-4F lowers hdl-inflammatory index in high-risk patients: a first-in-human multiple-dose, randomized controlled trial. Clin. Transl. Sci., 2017, 10(6), 455-469.
[28]
Vigna, G.B.; Satta, E.; Bernini, F.; Boarini, S.; Bosi, C.; Giusto, L.; Pinotti, E.; Tarugi, P.; Vanini, A.; Volpato, S.; Zimetti, F.; Zuliani, G.; Favari, E. Flow-mediated dilation, carotid wall thickness and HDL function in subjects with hyperalphalipoproteinemia. Nutr. Metab. Cardiovasc. Dis., 2014, 24(7), 777-783.
[29]
van der Steeg, W.A.; Holme, I.; Boekholdt, S.M.; Larsen, M.L.; Lindahl, C.; Stroes, E.S.; Tikkanen, M.J.; Wareham, N.J.; Faergeman, O.; Olsson, A.G.; Pedersen, T.R.; Khaw, K.T.; Kastelein, J.J. High-density lipoprotein cholesterol, high-density lipoprotein particle size, and apolipoprotein A-I: significance for cardiovascular risk: the IDEAL and EPIC-Norfolk studies. J. Am. Coll. Cardiol., 2008, 51(6), 634-642.
[30]
Madsen, C.M.; Varbo, A.; Nordestgaard, B.G. Extreme high high-density lipoprotein cholesterol is paradoxically associated with high mortality in men and women: two prospective cohort studies. Eur. Heart J., 2017, 38(32), 2478-2486.
[31]
Kontush, A.; Lindahl, M.; Lhomme, M.; Calabresi, L.; Chapman, M.J.; Davidson, W.S. Structure of HDL: particle subclasses and molecular components. Handb. Exp. Pharmacol., 2015, 224, 3-51.
[32]
Chan, D.C.; Ng, T.W.; Watts, G.F. Apolipoprotein A-II: evaluating its significance in dyslipidaemia, insulin resistance, and atherosclerosis. Ann. Med., 2012, 44(4), 313-324.
[33]
Rosenson, R.S.; Brewer, H.B., Jr; Chapman, M.J.; Fazio, S.; Hussain, M.M.; Kontush, A.; Krauss, R.M.; Otvos, J.D.; Remaley, A.T.; Schaefer, E.J. HDL measures, particle heterogeneity, proposed nomenclature, and relation to atherosclerotic cardiovascular events. Clin. Chem., 2011, 57(3), 392-410.
[34]
Davidson, W.S.; Silva, R.A.; Chantepie, S.; Lagor, W.R.; Chapman, M.J.; Kontush, A. Proteomic analysis of defined HDL subpopulations reveals particle-specific protein clusters: relevance to antioxidative function. Arterioscler. Thromb. Vasc. Biol., 2009, 29(6), 870-876.
[35]
Schaefer, E.J.; Foster, D.M.; Jenkins, L.L.; Lindgren, F.T.; Berman, M.; Levy, R.I.; Brewer, H.B., Jr The composition and metabolism of high density lipoprotein subfractions. Lipids, 1979, 14(5), 511-522.
[36]
Mahley, R.W.; Huang, Y.; Weisgraber, K.H. Putting cholesterol in its place: apoE and reverse cholesterol transport. J. Clin. Invest., 2006, 116(5), 1226-1229.
[37]
Kontush, A.; Therond, P.; Zerrad, A.; Couturier, M.; Négre-Salvayre, A.; de Souza, J.A.; Chantepie, S.; Chapman, M.J. Preferential sphingosine-1-phosphate enrichment and sphingomyelin depletion are key features of small dense HDL3 particles: relevance to antiapoptotic and antioxidative activities. Arterioscler. Thromb. Vasc. Biol., 2007, 27(8), 1843-1849.
[38]
Rader, D.J. Molecular regulation of HDL metabolism and function: implications for novel therapies. J. Clin. Invest., 2006, 116(12), 3090-3100.
[39]
von Eckardstein, A.; Nofer, J.R.; Assmann, G. High density lipoproteins and arteriosclerosis. Role of cholesterol efflux and reverse cholesterol transport. Arterioscler. Thromb. Vasc. Biol., 2001, 21(1), 13-27.
[40]
Lewis, G.F.; Rader, D.J. New insights into the regulation of HDL metabolism and reverse cholesterol transport. Circ. Res., 2005, 96(12), 1221-1232.
[41]
Wang, N.; Lan, D.; Chen, W.; Matsuura, F.; Tall, A.R. ATP-binding cassette transporters G1 and G4 mediate cellular cholesterol efflux to high-density lipoproteins. Proc. Natl. Acad. Sci. USA, 2004, 101(26), 9774-9779.
[42]
Kontush, A.; Chapman, M.J. Antiatherogenic small, dense HDL--guardian angel of the arterial wall. Nat. Clin. Pract. Cardiovasc. Med., 2006, 3(3), 144-153.
[43]
Asztalos, B.F.; de la Llera-Moya, M.; Dallal, G.E.; Horvath, K.V.; Schaefer, E.J.; Rothblat, G.H. Differential effects of HDL subpopulations on cellular ABCA1- and SR-BI-mediated cholesterol efflux. J. Lipid Res., 2005, 46(10), 2246-2253.
[44]
Assmann, G.; Nofer, J.R. Atheroprotective effects of high-density lipoproteins. Annu. Rev. Med., 2003, 54, 321-341.
[45]
Barter, P.J.; Nicholls, S.; Rye, K.A.; Anantharamaiah, G.M.; Navab, M.; Fogelman, A.M. Anti-inflammatory properties of HDL. Circ. Res., 2004, 95(8), 764-772.
[46]
Cockerill, G.W.; Rye, K.A.; Gamble, J.R.; Vadas, M.A.; Barter, P.J. High-density lipoproteins inhibit cytokine-induced expression of endothelial cell adhesion molecules. Arterioscler. Thromb. Vasc. Biol., 1995, 15(11), 1987-1994.
[47]
Nofer, J.R.; Geigenmüller, S.; Göpfert, C.; Assmann, G.; Buddecke, E.; Schmidt, A. High density lipoprotein-associated lysosphingolipids reduce E-selectin expression in human endothelial cells. Biochem. Biophys. Res. Commun., 2003, 310(1), 98-103.
[48]
Barter, P.J.; Baker, P.W.; Rye, K.A. Effect of high-density lipoproteins on the expression of adhesion molecules in endothelial cells. Curr. Opin. Lipidol., 2002, 13(3), 285-288.
[49]
Tölle, M.; Pawlak, A.; Schuchardt, M.; Kawamura, A.; Tietge, U.J.; Lorkowski, S.; Keul, P.; Assmann, G.; Chun, J.; Levkau, B.; van der Giet, M.; Nofer, J.R. HDL-associated lysosphingolipids inhibit NAD(P)H oxidase-dependent monocyte chemoattractant protein-1 production. Arterioscler. Thromb. Vasc. Biol., 2008, 28(8), 1542-1548.
[50]
Bursill, C.A.; Castro, M.L.; Beattie, D.T.; Nakhla, S.; van der Vorst, E.; Heather, A.K.; Barter, P.J.; Rye, K.A. High-density lipoproteins suppress chemokines and chemokine receptors in vitro and in vivo. Arterioscler. Thromb. Vasc. Biol., 2010, 30(9), 1773-1778.
[51]
Norata, G.D.; Pellegatta, F.; Hamsten, A.; Catapano, A.L.; Eriksson, P. Effects of HDL3 on the expression of matrix-degrading proteases in human endothelial cells. Int. J. Mol. Med., 2003, 12(1), 73-78.
[52]
Norata, G.D.; Björk, H.; Hamsten, A.; Catapano, A.L.; Eriksson, P. High-density lipoprotein subfraction 3 decreases ADAMTS-1 expression induced by lipopolysaccharide and tumor necrosis factor-alpha in human endothelial cells. Matrix Biol., 2004, 22(7), 557-560.
[53]
Norata, G.D.; Callegari, E.; Marchesi, M.; Chiesa, G.; Eriksson, P.; Catapano, A.L. High-density lipoproteins induce transforming growth factor-beta2 expression in endothelial cells. Circul., 2005, 111(21), 2805-2811.
[54]
Norata, G.D.; Marchesi, P.; Pirillo, A.; Uboldi, P.; Chiesa, G.; Maina, V.; Garlanda, C.; Mantovani, A.; Catapano, A.L. Long pentraxin 3, a key component of innate immunity, is modulated by high-density lipoproteins in endothelial cells. Arterioscler. Thromb. Vasc. Biol., 2008, 28(5), 925-931.
[55]
Murphy, A.J.; Woollard, K.J.; Hoang, A.; Mukhamedova, N.; Stirzaker, R.A.; McCormick, S.P.; Remaley, A.T.; Sviridov, D.; Chin-Dusting, J. High-density lipoprotein reduces the human monocyte inflammatory response. Arterioscler. Thromb. Vasc. Biol., 2008, 28(11), 2071-2077.
[56]
Thacker, S.G.; Zarzour, A.; Chen, Y.; Alcicek, M.S.; Freeman, L.A.; Sviridov, D.O.; Demosky, S.J., Jr; Remaley, A.T. High-density lipoprotein reduces inflammation from cholesterol crystals by inhibiting inflammasome activation. Immunol., 2016, 149(3), 306-319.
[57]
Baker, P.W.; Rye, K.A.; Gamble, J.R.; Vadas, M.A.; Barter, P.J. Phospholipid composition of reconstituted high density lipoproteins influences their ability to inhibit endothelial cell adhesion molecule expression. J. Lipid Res., 2000, 41(8), 1261-1267.
[58]
Kontush, A.; Chantepie, S.; Chapman, M.J. Small, dense HDL particles exert potent protection of atherogenic LDL against oxidative stress. Arterioscler. Thromb. Vasc. Biol., 2003, 23(10), 1881-1888.
[59]
de Souza, J.A.; Vindis, C.; Nègre-Salvayre, A.; Rye, K.A.; Couturier, M.; Therond, P.; Chantepie, S.; Salvayre, R.; Chapman, M.J.; Kontush, A. Small, dense HDL 3 particles attenuate apoptosis in endothelial cells: pivotal role of apolipoprotein A-I. J. Cell. Mol. Med., 2010, 14(3), 608-620.
[60]
Kontush, A.; Chapman, M.J. Antiatherogenic function of HDL particle subpopulations: focus on antioxidative activities. Curr. Opin. Lipidol., 2010, 21(4), 312-318.
[61]
Baker, P.W.; Rye, K.A.; Gamble, J.R.; Vadas, M.A.; Barter, P.J. Ability of reconstituted high density lipoproteins to inhibit cytokine-induced expression of vascular cell adhesion molecule-1 in human umbilical vein endothelial cells. J. Lipid Res., 1999, 40(2), 345-353.
[62]
Nobécourt, E.; Tabet, F.; Lambert, G.; Puranik, R.; Bao, S.; Yan, L.; Davies, M.J.; Brown, B.E.; Jenkins, A.J.; Dusting, G.J.; Bonnet, D.J.; Curtiss, L.K.; Barter, P.J.; Rye, K.A. Nonenzymatic glycation impairs the antiinflammatory properties of apolipoprotein A-I. Arterioscler. Thromb. Vasc. Biol., 2010, 30(4), 766-772.
[63]
Pirillo, A.; Uboldi, P.; Bolego, C.; Kuhn, H.; Catapano, A.L. The 15-lipoxygenase-modified high density lipoproteins 3 fail to inhibit the TNF-alpha-induced inflammatory response in human endothelial cells. J. Immunol., 2008, 181(4), 2821-2830.
[64]
Kameda, T.; Ohkawa, R.; Yano, K.; Usami, Y.; Miyazaki, A.; Matsuda, K.; Kawasaki, K.; Sugano, M.; Kubota, T.; Tozuka, M. Effects of Myeloperoxidase-Induced Oxidation on Antiatherogenic Functions of High-Density Lipoprotein. J. Lipids, 2015, 2015, 592594.
[65]
Undurti, A.; Huang, Y.; Lupica, J.A.; Smith, J.D.; DiDonato, J.A.; Hazen, S.L. Modification of high density lipoprotein by myeloperoxidase generates a pro-inflammatory particle. J. Biol. Chem., 2009, 284(45), 30825-30835.
[66]
Wendel, M.; Paul, R.; Heller, A.R. Lipoproteins in inflammation and sepsis. II. Clinical aspects. Intensive Care Med., 2007, 33(1), 25-35.
[67]
Birjmohun, R.S.; van Leuven, S.I.; Levels, J.H.; van ’t Veer, C.; Kuivenhoven, J.A.; Meijers, J.C.; Levi, M.; Kastelein, J.J.; van der Poll, T.; Stroes, E.S. High-density lipoprotein attenuates inflammation and coagulation response on endotoxin challenge in humans. Arterioscler. Thromb. Vasc. Biol., 2007, 27(5), 1153-1158.
[68]
Levels, J.H.; Geurts, P.; Karlsson, H.; Marée, R.; Ljunggren, S.; Fornander, L.; Wehenkel, L.; Lindahl, M.; Stroes, E.S.; Kuivenhoven, J.A.; Meijers, J.C. High-density lipoprotein proteome dynamics in human endotoxemia. Proteome Sci., 2011, 9(1), 34.
[69]
Norata, G.D.; Pirillo, A.; Ammirati, E.; Catapano, A.L. Emerging role of high density lipoproteins as a player in the immune system. Atheroscler., 2012, 220(1), 11-21.
[70]
Norata, G.D.; Pirillo, A.; Catapano, A.L. HDLs, immunity, and atherosclerosis. Curr. Opin. Lipidol., 2011, 22(5), 410-416.
[71]
Catapano, A.L.; Pirillo, A.; Bonacina, F.; Norata, G.D. HDL in innate and adaptive immunity. Cardiovasc. Res., 2014, 103(3), 372-383.
[72]
Watson, A.D.; Berliner, J.A.; Hama, S.Y.; La Du, B.N.; Faull, K.F.; Fogelman, A.M.; Navab, M. Protective effect of high density lipoprotein associated paraoxonase. Inhibition of the biological activity of minimally oxidized low density lipoprotein. J. Clin. Invest., 1995, 96(6), 2882-2891.
[73]
Uittenbogaard, A.; Shaul, P.W.; Yuhanna, I.S.; Blair, A.; Smart, E.J. High density lipoprotein prevents oxidized low density lipoprotein-induced inhibition of endothelial nitric-oxide synthase localization and activation in caveolae. J. Biol. Chem., 2000, 275(15), 11278-11283.
[74]
Badrnya, S.; Assinger, A.; Volf, I. Native high density lipoproteins (HDL) interfere with platelet activation induced by oxidized low density lipoproteins (OxLDL). Int. J. Mol. Sci., 2013, 14(5), 10107-10121.
[75]
Suc, I.; Escargueil-Blanc, I.; Troly, M.; Salvayre, R.; Nègre-Salvayre, A. HDL and ApoA prevent cell death of endothelial cells induced by oxidized LDL. Arterioscler. Thromb. Vasc. Biol., 1997, 17(10), 2158-2166.
[76]
Robbesyn, F.; Garcia, V.; Auge, N.; Vieira, O.; Frisach, M.F.; Salvayre, R.; Negre-Salvayre, A. HDL counterbalance the proinflammatory effect of oxidized LDL by inhibiting intracellular reactive oxygen species rise, proteasome activation, and subsequent NF-kappaB activation in smooth muscle cells. FASEB J., 2003, 17(6), 743-745.
[77]
Bancells, C.; Sánchez-Quesada, J.L.; Birkelund, R.; Ordóñez-Llanos, J.; Benítez, S. HDL and electronegative LDL exchange anti- and pro-inflammatory properties. J. Lipid Res., 2010, 51(10), 2947-2956.
[78]
Parthasarathy, S.; Barnett, J.; Fong, L.G. High-density lipoprotein inhibits the oxidative modification of low-density lipoprotein. Biochim. Biophys. Acta, 1990, 1044(2), 275-283.
[79]
Mackness, M.I.; Abbott, C.; Arrol, S.; Durrington, P.N. The role of high-density lipoprotein and lipid-soluble antioxidant vitamins in inhibiting low-density lipoprotein oxidation. Biochem. J., 1993, 294(Pt 3), 829-834.
[80]
Garner, B.; Waldeck, A.R.; Witting, P.K.; Rye, K.A.; Stocker, R. Oxidation of high density lipoproteins. II. Evidence for direct reduction of lipid hydroperoxides by methionine residues of apolipoproteins AI and AII. J. Biol. Chem., 1998, 273(11), 6088-6095.
[81]
Zerrad-Saadi, A.; Therond, P.; Chantepie, S.; Couturier, M.; Rye, K.A.; Chapman, M.J.; Kontush, A. HDL3-mediated inactivation of LDL-associated phospholipid hydroperoxides is determined by the redox status of apolipoprotein A-I and HDL particle surface lipid rigidity: relevance to inflammation and atherogenesis. Arterioscler. Thromb. Vasc. Biol., 2009, 29(12), 2169-2175.
[82]
Khoo, J.C.; Miller, E.; McLoughlin, P.; Steinberg, D. Prevention of low density lipoprotein aggregation by high density lipoprotein or apolipoprotein A-I. J. Lipid Res., 1990, 31(4), 645-652.
[83]
Sacre, S.M.; Stannard, A.K.; Owen, J.S.; Apolipoprotein, E. Apolipoprotein E (apoE) isoforms differentially induce nitric oxide production in endothelial cells. FEBS Lett., 2003, 540(1-3), 181-187.
[84]
Ostos, M.A.; Conconi, M.; Vergnes, L.; Baroukh, N.; Ribalta, J.; Girona, J.; Caillaud, J.M.; Ochoa, A.; Zakin, M.M. Antioxidative and antiatherosclerotic effects of human apolipoprotein A-IV in apolipoprotein E-deficient mice. Arterioscler. Thromb. Vasc. Biol., 2001, 21(6), 1023-1028.
[85]
Podrez, E.A. Anti-oxidant properties of high-density lipoprotein and atherosclerosis. Clin. Exp. Pharmacol. Physiol., 2010, 37(7), 719-725.
[86]
Drew, B.G.; Fidge, N.H.; Gallon-Beaumier, G.; Kemp, B.E.; Kingwell, B.A. High-density lipoprotein and apolipoprotein AI increase endothelial NO synthase activity by protein association and multisite phosphorylation. Proc. Natl. Acad. Sci. USA, 2004, 101(18), 6999-7004.
[87]
Yuhanna, I.S.; Zhu, Y.; Cox, B.E.; Hahner, L.D.; Osborne-Lawrence, S.; Lu, P.; Marcel, Y.L.; Anderson, R.G.; Mendelsohn, M.E.; Hobbs, H.H.; Shaul, P.W. High-density lipoprotein binding to scavenger receptor-BI activates endothelial nitric oxide synthase. Nat. Med., 2001, 7(7), 853-857.
[88]
Mineo, C.; Yuhanna, I.S.; Quon, M.J.; Shaul, P.W. High density lipoprotein-induced endothelial nitric-oxide synthase activation is mediated by Akt and MAP kinases. J. Biol. Chem., 2003, 278(11), 9142-9149.
[89]
Mineo, C.; Shaul, P.W. Regulation of eNOS in caveolae. Adv. Exp. Med. Biol., 2012, 729, 51-62.
[90]
Norata, G.D.; Callegari, E.; Inoue, H.; Catapano, A.L. HDL3 induces cyclooxygenase-2 expression and prostacyclin release in human endothelial cells via a p38 MAPK/CRE-dependent pathway: effects on COX-2/PGI-synthase coupling. Arterioscler. Thromb. Vasc. Biol., 2004, 24(5), 871-877.
[91]
de Beer, M.C.; Durbin, D.M.; Cai, L.; Jonas, A.; de Beer, F.C.; van der Westhuyzen, D.R. Apolipoprotein A-I conformation markedly influences HDL interaction with scavenger receptor BI. J. Lipid Res., 2001, 42(2), 309-313.
[92]
Nofer, J.R.; van der Giet, M.; Tölle, M.; Wolinska, I.; von Wnuck Lipinski, K.; Baba, H.A.; Tietge, U.J.; Gödecke, A.; Ishii, I.; Kleuser, B.; Schäfers, M.; Fobker, M.; Zidek, W.; Assmann, G.; Chun, J.; Levkau, B. HDL induces NO-dependent vasorelaxation via the lysophospholipid receptor S1P3. J. Clin. Invest., 2004, 113(4), 569-581.
[93]
Sattler, K.; Levkau, B. Sphingosine-1-phosphate as a mediator of high-density lipoprotein effects in cardiovascular protection. Cardiovasc. Res., 2009, 82(2), 201-211.
[94]
Besler, C.; Heinrich, K.; Rohrer, L.; Doerries, C.; Riwanto, M.; Shih, D.M.; Chroni, A.; Yonekawa, K.; Stein, S.; Schaefer, N.; Mueller, M.; Akhmedov, A.; Daniil, G.; Manes, C.; Templin, C.; Wyss, C.; Maier, W.; Tanner, F.C.; Matter, C.M.; Corti, R.; Furlong, C.; Lusis, A.J.; von Eckardstein, A.; Fogelman, A.M.; Lüscher, T.F.; Landmesser, U. Mechanisms underlying adverse effects of HDL on eNOS-activating pathways in patients with coronary artery disease. J. Clin. Invest., 2011, 121(7), 2693-2708.
[95]
Oravec, S.; Demuth, K.; Myara, I.; Hornych, A. The effect of high density lipoprotein subfractions on endothelial eicosanoid secretion. Thromb. Res., 1998, 92(2), 65-71.
[96]
Bombeli, T.; Karsan, A.; Tait, J.F.; Harlan, J.M. Apoptotic vascular endothelial cells become procoagulant. Blood, 1997, 89(7), 2429-2442.
[97]
Kockx, M.M.; Herman, A.G. Apoptosis in atherosclerosis: beneficial or detrimental? Cardiovasc. Res., 2000, 45(3), 736-746.
[98]
Feuerborn, R.; Becker, S.; Potì, F.; Nagel, P.; Brodde, M.; Schmidt, H.; Christoffersen, C.; Ceglarek, U.; Burkhardt, R.; Nofer, J.R. High density lipoprotein (HDL)-associated sphingosine 1-phosphate (S1P) inhibits macrophage apoptosis by stimulating STAT3 activity and survivin expression. Atheroscler., 2017, 257, 29-37.
[99]
Nofer, J.R.; Levkau, B.; Wolinska, I.; Junker, R.; Fobker, M.; von Eckardstein, A.; Seedorf, U.; Assmann, G. Suppression of endothelial cell apoptosis by high density lipoproteins (HDL) and HDL-associated lysosphingolipids. J. Biol. Chem., 2001, 276(37), 34480-34485.
[100]
Sugano, M.; Tsuchida, K.; Makino, N. High-density lipoproteins protect endothelial cells from tumor necrosis factor-alpha-induced apoptosis. Biochem. Biophys. Res. Commun., 2000, 272(3), 872-876.
[101]
Kimura, T.; Sato, K.; Kuwabara, A.; Tomura, H.; Ishiwara, M.; Kobayashi, I.; Ui, M.; Okajima, F. Sphingosine 1-phosphate may be a major component of plasma lipoproteins responsible for the cytoprotective actions in human umbilical vein endothelial cells. J. Biol. Chem., 2001, 276(34), 31780-31785.
[102]
Terasaka, N.; Wang, N.; Yvan-Charvet, L.; Tall, A.R. High-density lipoprotein protects macrophages from oxidized low-density lipoprotein-induced apoptosis by promoting efflux of 7-ketocholesterol via ABCG1. Proc. Natl. Acad. Sci. USA, 2007, 104(38), 15093-15098.
[103]
Theilmeier, G.; Schmidt, C.; Herrmann, J.; Keul, P.; Schäfers, M.; Herrgott, I.; Mersmann, J.; Larmann, J.; Hermann, S.; Stypmann, J.; Schober, O.; Hildebrand, R.; Schulz, R.; Heusch, G.; Haude, M.; von Wnuck Lipinski, K.; Herzog, C.; Schmitz, M.; Erbel, R.; Chun, J.; Levkau, B. High-density lipoproteins and their constituent, sphingosine-1-phosphate, directly protect the heart against ischemia/reperfusion injury in vivo via the S1P3 lysophospholipid receptor. Circul., 2006, 114(13), 1403-1409.
[104]
Frias, M.A.; Lang, U.; Gerber-Wicht, C.; James, R.W. Native and reconstituted HDL protect cardiomyocytes from doxorubicin-induced apoptosis. Cardiovasc. Res., 2010, 85(1), 118-126.
[105]
Fuhrman, B.; Gantman, A.; Aviram, M. Paraoxonase 1 (PON1) deficiency in mice is associated with reduced expression of macrophage SR-BI and consequently the loss of HDL cytoprotection against apoptosis. Atheroscler., 2010, 211(1), 61-68.
[106]
Brodeur, M.R.; Brissette, L.; Falstrault, L.; Moreau, R. HDL3 reduces the association and modulates the metabolism of oxidized LDL by osteoblastic cells: a protection against cell death. J. Cell. Biochem., 2008, 105(6), 1374-1385.
[107]
Pellegatta, F.; Bragheri, M.; Grigore, L.; Raselli, S.; Maggi, F.M.; Brambilla, C.; Reduzzi, A.; Pirillo, A.; Norata, G.D.; Catapano, A.L. In vitro isolation of circulating endothelial progenitor cells is related to the high density lipoprotein plasma levels. Int. J. Mol. Med., 2006, 17(2), 203-208.
[108]
Lerch, P.G.; Spycher, M.O.; Doran, J.E. Reconstituted high density lipoprotein (rHDL) modulates platelet activity in vitro and ex vivo. Thromb. Haemost., 1998, 80(2), 316-320.
[109]
Viswambharan, H.; Ming, X.F.; Zhu, S.; Hubsch, A.; Lerch, P.; Vergères, G.; Rusconi, S.; Yang, Z. Reconstituted high-density lipoprotein inhibits thrombin-induced endothelial tissue factor expression through inhibition of RhoA and stimulation of phosphatidylinositol 3-kinase but not Akt/endothelial nitric oxide synthase. Circ. Res., 2004, 94(7), 918-925.
[110]
Pomerantz, K.B.; Fleisher, L.N.; Tall, A.R.; Cannon, P.J. Enrichment of endothelial cell arachidonate by lipid transfer from high density lipoproteins: relationship to prostaglandin I2 synthesis. J. Lipid Res., 1985, 26(10), 1269-1276.
[111]
Chung, D.W.; Chen, J.; Ling, M.; Fu, X.; Blevins, T.; Parsons, S.; Le, J.; Harris, J.; Martin, T.R.; Konkle, B.A.; Zheng, Y.; López, J.A. High-density lipoprotein modulates thrombosis by preventing von Willebrand factor self-association and subsequent platelet adhesion. Blood, 2016, 127(5), 637-645.
[112]
Norata, G.D.; Pirillo, A.; Catapano, A.L. Modified, HDL biological and physiopathological consequences. Nutr. Metab. Cardiovasc. Dis., 2006, 16(5), 371-386.
[113]
Annema, W.; Tietge, U.J. Role of hepatic lipase and endothelial lipase in high-density lipoprotein-mediated reverse cholesterol transport. Curr. Atheroscler. Rep., 2011, 13(3), 257-265.
[114]
Schilcher, I.; Kern, S.; Hrzenjak, A.; Eichmann, T.O.; Stojakovic, T.; Scharnagl, H.; Duta-Mare, M.; Kratky, D.; Marsche, G.; Frank, S. Impact of endothelial lipase on cholesterol efflux capacity of serum and high-density lipoprotein. Sci. Rep., 2017, 7(1), 12485.
[115]
Calabresi, L.; Franceschini, G. Lecithin:cholesterol acyltransferase, high-density lipoproteins, and atheroprotection in humans. Trends Cardiovasc. Med., 2010, 20(2), 50-53.
[116]
Lucero, D.; Sviridov, D.; Freeman, L.; López, G.I.; Fassio, E.; Remaley, A.T.; Schreier, L. Increased cholesterol efflux capacity in metabolic syndrome: Relation with qualitative alterations in HDL and LCAT. Atheroscler., 2015, 242(1), 236-242.
[117]
Awadallah, S.; Madkour, M.; Hamidi, R.A.; Alwafa, E.A.; Hattab, M.; Zakkour, B.; Al-Matroushi, A.; Ahmed, E.; Al-Kitbi, M. Plasma levels of Apolipoprotein A1 and Lecithin:Cholesterol Acyltransferase in type 2 diabetes mellitus: Correlations with haptoglobin phenotypes. Diabetes Metab. Syndr., 2017, 11(Suppl. 2), S543-S546.
[118]
Calabresi, L.; Simonelli, S.; Conca, P.; Busnach, G.; Cabibbe, M.; Gesualdo, L.; Gigante, M.; Penco, S.; Veglia, F.; Franceschini, G. Acquired lecithin:cholesterol acyltransferase deficiency as a major factor in lowering plasma HDL levels in chronic kidney disease. J. Intern. Med., 2015, 277(5), 552-561.
[119]
Calabresi, L.; Simonelli, S.; Gomaraschi, M.; Franceschini, G. Genetic lecithin: cholesterol acyltransferase deficiency and cardiovascular disease. Atheroscler., 2012, 222(2), 299-306.
[120]
Calabresi, L.; Favari, E.; Moleri, E.; Adorni, M.P.; Pedrelli, M.; Costa, S.; Jessup, W.; Gelissen, I.C.; Kovanen, P.T.; Bernini, F.; Franceschini, G. Functional LCAT is not required for macrophage cholesterol efflux to human serum. Atheroscler., 2009, 204(1), 141-146.
[121]
van den Bogaard, B.; Holleboom, A.G.; Duivenvoorden, R.; Hutten, B.A.; Kastelein, J.J.; Hovingh, G.K.; Kuivenhoven, J.A.; Stroes, E.S.; van den Born, B.J. Patients with low HDL-cholesterol caused by mutations in LCAT have increased arterial stiffness. Atheroscler., 2012, 225(2), 481-485.
[122]
Barter, P.J.; Brewer, H.B., Jr; Chapman, M.J.; Hennekens, C.H.; Rader, D.J.; Tall, A.R. Cholesteryl ester transfer protein: a novel target for raising HDL and inhibiting atherosclerosis. Arterioscler. Thromb. Vasc. Biol., 2003, 23(2), 160-167.
[123]
Thompson, A.; Di Angelantonio, E.; Sarwar, N.; Erqou, S.; Saleheen, D.; Dullaart, R.P.; Keavney, B.; Ye, Z.; Danesh, J. Association of cholesteryl ester transfer protein genotypes with CETP mass and activity, lipid levels, and coronary risk. JAMA, 2008, 299(23), 2777-2788.
[124]
Johannsen, T.H.; Frikke-Schmidt, R.; Schou, J.; Nordestgaard, B.G.; Tybjærg-Hansen, A. Genetic inhibition of CETP, ischemic vascular disease and mortality, and possible adverse effects. J. Am. Coll. Cardiol., 2012, 60(20), 2041-2048.
[125]
Mabuchi, H.; Nohara, A.; Inazu, A. Cholesteryl ester transfer protein (CETP) deficiency and CETP inhibitors. Mol. Cells, 2014, 37(11), 777-784.
[126]
Matsuura, F.; Wang, N.; Chen, W.; Jiang, X.C.; Tall, A.R. HDL from CETP-deficient subjects shows enhanced ability to promote cholesterol efflux from macrophages in an apoE- and ABCG1-dependent pathway. J. Clin. Invest., 2006, 116(5), 1435-1442.
[127]
Miwa, K.; Inazu, A.; Kawashiri, M.; Nohara, A.; Higashikata, T.; Kobayashi, J.; Koizumi, J.; Nakajima, K.; Nakano, T.; Niimi, M.; Mabuchi, H.; Yamagishi, M. Cholesterol efflux from J774 macrophages and Fu5AH hepatoma cells to serum is preserved in CETP-deficient patients. Clin. Chim. Acta, 2009, 402(1-2), 19-24.
[128]
Gomaraschi, M.; Ossoli, A.; Pozzi, S.; Nilsson, P.; Cefalù, A.B.; Averna, M.; Kuivenhoven, J.A.; Hovingh, G.K.; Veglia, F.; Franceschini, G.; Calabresi, L. eNOS activation by HDL is impaired in genetic CETP deficiency. PLoS One, 2014, 9(5), e95925.
[129]
Chantepie, S.; Bochem, A.E.; Chapman, M.J.; Hovingh, G.K.; Kontush, A. High-density lipoprotein (HDL) particle subpopulations in heterozygous cholesteryl ester transfer protein (CETP) deficiency: maintenance of antioxidative activity. PLoS One, 2012, 7(11), e49336.
[130]
Rinninger, F.; Brundert, M.; Budzinski, R.M.; Fruchart, J.C.; Greten, H.; Castro, G.R. Scavenger receptor BI (SR-BI) mediates a higher selective cholesteryl ester uptake from LpA-I compared with LpA-I:A-II lipoprotein particles. Atheroscler., 2003, 166(1), 31-40.
[131]
Lüscher, T.F.; Taddei, S.; Kaski, J.C.; Jukema, J.W.; Kallend, D.; Münzel, T.; Kastelein, J.J.; Deanfield, J.E. Vascular effects and safety of dalcetrapib in patients with or at risk of coronary heart disease: the dal-VESSEL randomized clinical trial. Eur. Heart J., 2012, 33(7), 857-865.
[132]
Ference, B.A.; Kastelein, J.J.P.; Ginsberg, H.N.; Chapman, M.J.; Nicholls, S.J.; Ray, K.K.; Packard, C.J.; Laufs, U.; Brook, R.D.; Oliver-Williams, C.; Butterworth, A.S.; Danesh, J.; Smith, G.D.; Catapano, A.L.; Sabatine, M.S. Association of genetic variants related to cetp inhibitors and statins with lipoprotein levels and cardiovascular risk. JAMA, 2017, 318(10), 947-956.
[133]
Simic, B.; Mocharla, P.; Crucet, M.; Osto, E.; Kratzer, A.; Stivala, S.; Kühnast, S.; Speer, T.; Doycheva, P.; Princen, H.M.; van der Hoorn, J.W.; Jukema, J.W.; Giral, H.; Tailleux, A.; Landmesser, U.; Staels, B.; Lüscher, T.F. Anacetrapib, but not evacetrapib, impairs endothelial function in CETP-transgenic mice in spite of marked HDL-C increase. Atheroscler., 2017, 257, 186-194.
[134]
Nicholls, S.J.; Ray, K.K.; Ballantyne, C.M.; Beacham, L.A.; Miller, D.L.; Ruotolo, G.; Nissen, S.E.; Riesmeyer, J.S.; Investigators, A. Comparative effects of cholesteryl ester transfer protein inhibition, statin or ezetimibe on lipid factors: The ACCENTUATE trial. Atheroscler., 2017, 261, 12-18.
[135]
Riwanto, M.; Rohrer, L.; Roschitzki, B.; Besler, C.; Mocharla, P.; Mueller, M.; Perisa, D.; Heinrich, K.; Altwegg, L.; von Eckardstein, A.; Lüscher, T.F.; Landmesser, U. Altered activation of endothelial anti- and proapoptotic pathways by high-density lipoprotein from patients with coronary artery disease: role of high-density lipoprotein-proteome remodeling. Circulation, 2013, 127(8), 891-904.
[136]
Luo, M.; Liu, A.; Wang, S.; Wang, T.; Hu, D.; Wu, S.; Peng, D. ApoCIII enrichment in HDL impairs HDL-mediated cholesterol efflux capacity. Sci. Rep., 2017, 7(1), 2312.
[137]
Tao, Y.; Xiong, Y.; Wang, H.; Chu, S.; Zhong, R.; Wang, J.; Wang, G.; Ren, X.; Yu, J. APOC3 induces endothelial dysfunction through TNF-α and JAM-1. Lipids Health Dis., 2016, 15(1), 153.
[138]
Zheng, C.; Azcutia, V.; Aikawa, E.; Figueiredo, J.L.; Croce, K.; Sonoki, H.; Sacks, F.M.; Luscinskas, F.W.; Aikawa, M. Statins suppress apolipoprotein CIII-induced vascular endothelial cell activation and monocyte adhesion. Eur. Heart J., 2013, 34(8), 615-624.
[139]
Kawakami, A.; Aikawa, M.; Alcaide, P.; Luscinskas, F.W.; Libby, P.; Sacks, F.M. Apolipoprotein CIII induces expression of vascular cell adhesion molecule-1 in vascular endothelial cells and increases adhesion of monocytic cells. Circulation, 2006, 114(7), 681-687.
[140]
Shao, B.; Oda, M.N.; Oram, J.F.; Heinecke, J.W. Myeloperoxidase: an oxidative pathway for generating dysfunctional high-density lipoprotein. Chem. Res. Toxicol., 2010, 23(3), 447-454.
[141]
Sugiyama, S.; Okada, Y.; Sukhova, G.K.; Virmani, R.; Heinecke, J.W.; Libby, P. Macrophage myeloperoxidase regulation by granulocyte macrophage colony-stimulating factor in human atherosclerosis and implications in acute coronary syndromes. Am. J. Pathol., 2001, 158(3), 879-891.
[142]
Ferrante, G.; Nakano, M.; Prati, F.; Niccoli, G.; Mallus, M.T.; Ramazzotti, V.; Montone, R.A.; Kolodgie, F.D.; Virmani, R.; Crea, F. High levels of systemic myeloperoxidase are associated with coronary plaque erosion in patients with acute coronary syndromes: a clinicopathological study. Circulation, 2010, 122(24), 2505-2513.
[143]
Huang, Y.; Wu, Z.; Riwanto, M.; Gao, S.; Levison, B.S.; Gu, X.; Fu, X.; Wagner, M.A.; Besler, C.; Gerstenecker, G.; Zhang, R.; Li, X.M.; DiDonato, A.J.; Gogonea, V.; Tang, W.H.; Smith, J.D.; Plow, E.F.; Fox, P.L.; Shih, D.M.; Lusis, A.J.; Fisher, E.A.; DiDonato, J.A.; Landmesser, U.; Hazen, S.L. Myeloperoxidase, paraoxonase-1, and HDL form a functional ternary complex. J. Clin. Invest., 2013, 123(9), 3815-3828.
[144]
Bergt, C.; Pennathur, S.; Fu, X.; Byun, J.; O’Brien, K.; McDonald, T.O.; Singh, P.; Anantharamaiah, G.M.; Chait, A.; Brunzell, J.; Geary, R.L.; Oram, J.F.; Heinecke, J.W. The myeloperoxidase product hypochlorous acid oxidizes HDL in the human artery wall and impairs ABCA1-dependent cholesterol transport. Proc. Natl. Acad. Sci. USA, 2004, 101(35), 13032-13037.
[145]
Pennathur, S.; Bergt, C.; Shao, B.; Byun, J.; Kassim, S.Y.; Singh, P.; Green, P.S.; McDonald, T.O.; Brunzell, J.; Chait, A.; Oram, J.F.; O’brien, K.; Geary, R.L.; Heinecke, J.W. Human atherosclerotic intima and blood of patients with established coronary artery disease contain high density lipoprotein damaged by reactive nitrogen species. J. Biol. Chem., 2004, 279(41), 42977-42983.
[146]
Lu, N.; Xie, S.; Li, J.; Tian, R.; Peng, Y.Y. Myeloperoxidase-mediated oxidation targets serum apolipoprotein A-I in diabetic patients and represents a potential mechanism leading to impaired anti-apoptotic activity of high density lipoprotein. Clin. Chim. Acta, 2015, 441, 163-170.
[147]
Shao, B.; Tang, C.; Sinha, A.; Mayer, P.S.; Davenport, G.D.; Brot, N.; Oda, M.N.; Zhao, X.Q.; Heinecke, J.W. Humans with atherosclerosis have impaired ABCA1 cholesterol efflux and enhanced high-density lipoprotein oxidation by myeloperoxidase. Circ. Res., 2014, 114(11), 1733-1742.
[148]
Zheng, L.; Nukuna, B.; Brennan, M.L.; Sun, M.; Goormastic, M.; Settle, M.; Schmitt, D.; Fu, X.; Thomson, L.; Fox, P.L.; Ischiropoulos, H.; Smith, J.D.; Kinter, M.; Hazen, S.L. Apolipoprotein A-I is a selective target for myeloperoxidase-catalyzed oxidation and functional impairment in subjects with cardiovascular disease. J. Clin. Invest., 2004, 114(4), 529-541.
[149]
Bergt, C.; Fu, X.; Huq, N.P.; Kao, J.; Heinecke, J.W. Lysine residues direct the chlorination of tyrosines in YXXK motifs of apolipoprotein A-I when hypochlorous acid oxidizes high density lipoprotein. J. Biol. Chem., 2004, 279(9), 7856-7866.
[150]
Shao, B.; Bergt, C.; Fu, X.; Green, P.; Voss, J.C.; Oda, M.N.; Oram, J.F.; Heinecke, J.W. Tyrosine 192 in apolipoprotein A-I is the major site of nitration and chlorination by myeloperoxidase, but only chlorination markedly impairs ABCA1-dependent cholesterol transport. J. Biol. Chem., 2005, 280(7), 5983-5993.
[151]
Shao, B.; Pennathur, S.; Heinecke, J.W. Myeloperoxidase targets apolipoprotein A-I, the major high density lipoprotein protein, for site-specific oxidation in human atherosclerotic lesions. J. Biol. Chem., 2012, 287(9), 6375-6386.
[152]
Hewing, B.; Parathath, S.; Barrett, T.; Chung, W.K.; Astudillo, Y.M.; Hamada, T.; Ramkhelawon, B.; Tallant, T.C.; Yusufishaq, M.S.; Didonato, J.A.; Huang, Y.; Buffa, J.; Berisha, S.Z.; Smith, J.D.; Hazen, S.L.; Fisher, E.A. Effects of native and myeloperoxidase-modified apolipoprotein a-I on reverse cholesterol transport and atherosclerosis in mice. Arterioscler. Thromb. Vasc. Biol., 2014, 34(4), 779-789.
[153]
Zhou, B.; Zu, L.; Chen, Y.; Zheng, X.; Wang, Y.; Pan, B.; Dong, M.; Zhou, E.; Zhao, M.; Zhang, Y.; Zheng, L.; Gao, W. Myeloperoxidase-oxidized high density lipoprotein impairs atherosclerotic plaque stability by inhibiting smooth muscle cell migration. Lipids Health Dis., 2017, 16(1), 3.
[154]
Khine, H.W.; Teiber, J.F.; Haley, R.W.; Khera, A.; Ayers, C.R.; Rohatgi, A. Association of the serum myeloperoxidase/high-density lipoprotein particle ratio and incident cardiovascular events in a multi-ethnic population: Observations from the Dallas Heart Study. Atheroscler., 2017, 263, 156-162.
[155]
Nathan, D.M.; Genuth, S.; Lachin, J.; Cleary, P.; Crofford, O.; Davis, M.; Rand, L.; Siebert, C. The effect of intensive treatment of diabetes on the development and progression of long-term complications in insulin-dependent diabetes mellitus. N. Engl. J. Med., 1993, 329(14), 977-986.
[156]
Srivastava, R.A.K. Dysfunctional HDL in diabetes mellitus and its role in the pathogenesis of cardiovascular disease. Mol. Cell. Biochem., 2017.
[157]
Matsunaga, T.; Iguchi, K.; Nakajima, T.; Koyama, I.; Miyazaki, T.; Inoue, I.; Kawai, S.; Katayama, S.; Hirano, K.; Hokari, S.; Komoda, T. Glycated high-density lipoprotein induces apoptosis of endothelial cells via a mitochondrial dysfunction. Biochem. Biophys. Res. Commun., 2001, 287(3), 714-720.
[158]
Matsunaga, T.; Nakajima, T.; Miyazaki, T.; Koyama, I.; Hokari, S.; Inoue, I.; Kawai, S.; Shimomura, H.; Katayama, S.; Hara, A.; Komoda, T. Glycated high-density lipoprotein regulates reactive oxygen species and reactive nitrogen species in endothelial cells. Metabol., 2003, 52(1), 42-49.
[159]
Brindisi, M.C.; Duvillard, L.; Monier, S.; Vergès, B.; Perségol, L. Deleterious effect of glycation on the ability of HDL to counteract the inhibitory effect of oxidized LDL on endothelium-dependent vasorelaxation. Diabetes Metab. Res. Rev., 2013, 29(8), 618-623.
[160]
Du, Q.; Qian, M.M.; Liu, P.L.; Zhang, L.; Wang, Y.; Liu, D.H. Glycation of high-density lipoprotein triggers oxidative stress and promotes the proliferation and migration of vascular smooth muscle cells. J. Geriatr. Cardiol., 2017, 14(7), 473-480.
[161]
Nobecourt, E.; Davies, M.J.; Brown, B.E.; Curtiss, L.K.; Bonnet, D.J.; Charlton, F.; Januszewski, A.S.; Jenkins, A.J.; Barter, P.J.; Rye, K.A. The impact of glycation on apolipoprotein A-I structure and its ability to activate lecithin:cholesterol acyltransferase. Diabetologia, 2007, 50(3), 643-653.
[162]
Hoang, A.; Murphy, A.J.; Coughlan, M.T.; Thomas, M.C.; Forbes, J.M.; O’Brien, R.; Cooper, M.E.; Chin-Dusting, J.P.; Sviridov, D. Advanced glycation of apolipoprotein A-I impairs its anti-atherogenic properties. Diabetologia, 2007, 50(8), 1770-1779.
[163]
Pu, L.J.; Lu, L.; Zhang, R.Y.; Du, R.; Shen, Y.; Zhang, Q.; Yang, Z.K.; Chen, Q.J.; Shen, W.F. Glycation of apoprotein A-I is associated with coronary artery plaque progression in type 2 diabetic patients. Diabetes Care, 2013, 36(5), 1312-1320.
[164]
Shen, Y.; Ding, F.H.; Sun, J.T.; Pu, L.J.; Zhang, R.Y.; Zhang, Q.; Chen, Q.J.; Shen, W.F.; Lu, L. Association of elevated apoA-I glycation and reduced HDL-associated paraoxonase1, 3 activity, and their interaction with angiographic severity of coronary artery disease in patients with type 2 diabetes mellitus. Cardiovasc. Diabetol., 2015, 14, 52.
[165]
Kashyap, S.R.; Osme, A.; Ilchenko, S.; Golizeh, M.; Lee, K.; Wang, S.; Bena, J.; Previs, S.F.; Smith, J.D.; Kasumov, T. Glycation Reduces the Stability of ApoAI and Increases HDL Dysfunction in Diet-controlled Type 2 Diabetes. J. Clin. Endocrinol. Metab., 2017.
[166]
Mastorikou, M.; Mackness, B.; Liu, Y.; Mackness, M. Glycation of paraoxonase-1 inhibits its activity and impairs the ability of high-density lipoprotein to metabolize membrane lipid hydroperoxides. Diabet. Med., 2008, 25(9), 1049-1055.
[167]
Perségol, L.; Vergès, B.; Foissac, M.; Gambert, P.; Duvillard, L. Inability of HDL from type 2 diabetic patients to counteract the inhibitory effect of oxidised LDL on endothelium-dependent vasorelaxation. Diabetologia, 2006, 49(6), 1380-1386.
[168]
Liu, D.; Ji, L.; Zhang, D.; Tong, X.; Pan, B.; Liu, P.; Zhang, Y.; Huang, Y.; Su, J.; Willard, B.; Zheng, L. Nonenzymatic glycation of high-density lipoprotein impairs its anti-inflammatory effects in innate immunity. Diabetes Metab. Res. Rev., 2012, 28(2), 186-195.
[169]
Pirillo, A.; Catapano, A.L.; Norata, G.D. HDL in infectious diseases and sepsis. Handb. Exp. Pharmacol., 2015, 224, 483-508.
[170]
Norata, G.D.; Pirillo, A.; Ammirati, E.; Catapano, A.L. Emerging role of high density lipoproteins as a player in the immune system. Atheroscler., 2012, 220(1), 11-21.
[171]
de la Llera Moya, M.; McGillicuddy, F.C.; Hinkle, C.C.; Byrne, M.; Joshi, M.R.; Nguyen, V.; Tabita-Martinez, J.; Wolfe, M.L.; Badellino, K.; Pruscino, L.; Mehta, N.N.; Asztalos, B.F.; Reilly, M.P. Inflammation modulates human HDL composition and function in vivo. Atheroscler., 2012, 222(2), 390-394.
[172]
Khovidhunkit, W.; Kim, M.S.; Memon, R.A.; Shigenaga, J.K.; Moser, A.H.; Feingold, K.R.; Grunfeld, C. Effects of infection and inflammation on lipid and lipoprotein metabolism: mechanisms and consequences to the host. J. Lipid Res., 2004, 45(7), 1169-1196.
[173]
Coetzee, G.A.; Strachan, A.F.; van der Westhuyzen, D.R.; Hoppe, H.C.; Jeenah, M.S.; de Beer, F.C. Serum amyloid A-containing human high density lipoprotein 3. Density, size, and apolipoprotein composition. J. Biol. Chem., 1986, 261(21), 9644-9651.
[174]
Uhlar, C.M.; Whitehead, A.S. Serum amyloid A, the major vertebrate acute-phase reactant. Eur. J. Biochem., 1999, 265(2), 501-523.
[175]
van Leeuwen, H.J.; Heezius, E.C.; Dallinga, G.M.; van Strijp, J.A.; Verhoef, J.; van Kessel, K.P. Lipoprotein metabolism in patients with severe sepsis. Crit. Care Med., 2003, 31(5), 1359-1366.
[176]
Feingold, K.R.; Memon, R.A.; Moser, A.H.; Grunfeld, C. Paraoxonase activity in the serum and hepatic mRNA levels decrease during the acute phase response. Atheroscler., 1998, 139(2), 307-315.
[177]
Van Lenten, B.J.; Hama, S.Y.; de Beer, F.C.; Stafforini, D.M.; McIntyre, T.M.; Prescott, S.M.; La Du, B.N.; Fogelman, A.M.; Navab, M. Anti-inflammatory HDL becomes pro-inflammatory during the acute phase response. Loss of protective effect of HDL against LDL oxidation in aortic wall cell cocultures. J. Clin. Invest., 1995, 96(6), 2758-2767.
[178]
Cao, Y.; Stafforini, D.M.; Zimmerman, G.A.; McIntyre, T.M.; Prescott, S.M. Expression of plasma platelet-activating factor acetylhydrolase is transcriptionally regulated by mediators of inflammation. J. Biol. Chem., 1998, 273(7), 4012-4020.
[179]
Memon, R.A.; Fuller, J.; Moser, A.H.; Feingold, K.R.; Grunfeld, C. In vivo regulation of plasma platelet-activating factor acetylhydrolase during the acute phase response. Am. J. Physiol., 1999, 277(1), R94-R103.
[180]
Badellino, K.O.; Wolfe, M.L.; Reilly, M.P.; Rader, D.J. Endothelial lipase is increased in vivo by inflammation in humans. Circulation, 2008, 117(5), 678-685.
[181]
Banka, C.L.; Yuan, T.; de Beer, M.C.; Kindy, M.; Curtiss, L.K.; de Beer, F.C. Serum amyloid A (SAA): influence on HDL-mediated cellular cholesterol efflux. J. Lipid Res., 1995, 36(5), 1058-1065.
[182]
McGillicuddy, F.C.; de la Llera Moya, M.; Hinkle, C.C.; Joshi, M.R.; Chiquoine, E.H.; Billheimer, J.T.; Rothblat, G.H.; Reilly, M.P. Inflammation impairs reverse cholesterol transport in vivo. Circulation, 2009, 119(8), 1135-1145.
[183]
Zimetti, F.; De Vuono, S.; Gomaraschi, M.; Adorni, M.P.; Favari, E.; Ronda, N.; Ricci, M.A.; Veglia, F.; Calabresi, L.; Lupattelli, G. Plasma cholesterol homeostasis, HDL remodeling and function during the acute phase reaction. J. Lipid Res., 2017, 58(10), 2051-2060.
[184]
Digre, A.; Nan, J.; Frank, M.; Li, J.P. Heparin interactions with apoA1 and SAA in inflammation-associated HDL. Biochem. Biophys. Res. Commun., 2016, 474(2), 309-314.
[185]
Hintenberger, R.; Falkinger, A.; Danninger, K.; Pieringer, H. Cardiovascular disease in patients with autoinflammatory syndromes. Rheumatol. Int., 2017, 38(1), 37-50.
[186]
Ammirati, E.; Bozzolo, E.P.; Contri, R.; Baragetti, A.; Palini, A.G.; Cianflone, D.; Banfi, M.; Uboldi, P.; Bottoni, G.; Scotti, I.; Pirillo, A.; Grigore, L.; Garlaschelli, K.; Monaco, C.; Catapano, A.L.; Sabbadini, M.G.; Manfredi, A.A.; Norata, G.D. Cardiometabolic and immune factors associated with increased common carotid artery intima-media thickness and cardiovascular disease in patients with systemic lupus erythematosus. Nutr. Metab. Cardiovasc. Dis., 2014, 24(7), 751-759.
[187]
Montecucco, F.; Favari, E.; Norata, G.D.; Ronda, N.; Nofer, J.R.; Vuilleumier, N. Impact of systemic inflammation and autoimmune diseases on apoA-I and HDL plasma levels and functions. Handb. Exp. Pharmacol., 2015, 224, 455-482.
[188]
Charles-Schoeman, C.; Lee, Y.Y.; Grijalva, V.; Amjadi, S.; FitzGerald, J.; Ranganath, V.K.; Taylor, M.; McMahon, M.; Paulus, H.E.; Reddy, S.T. Cholesterol efflux by high density lipoproteins is impaired in patients with active rheumatoid arthritis. Ann. Rheum. Dis., 2012, 71(7), 1157-1162.
[189]
Ronda, N.; Favari, E.; Borghi, M.O.; Ingegnoli, F.; Gerosa, M.; Chighizola, C.; Zimetti, F.; Adorni, M.P.; Bernini, F.; Meroni, P.L. Impaired serum cholesterol efflux capacity in rheumatoid arthritis and systemic lupus erythematosus. Ann. Rheum. Dis., 2014, 73(3), 609-615.
[190]
McMahon, M.; Grossman, J.; FitzGerald, J.; Dahlin-Lee, E.; Wallace, D.J.; Thong, B.Y.; Badsha, H.; Kalunian, K.; Charles, C.; Navab, M.; Fogelman, A.M.; Hahn, B.H. Proinflammatory high-density lipoprotein as a biomarker for atherosclerosis in patients with systemic lupus erythematosus and rheumatoid arthritis. Arthritis Rheum., 2006, 54(8), 2541-2549.
[191]
Smith, C.K.; Seto, N.L.; Vivekanandan-Giri, A.; Yuan, W.; Playford, M.P.; Manna, Z.; Hasni, S.A.; Kuai, R.; Mehta, N.N.; Schwendeman, A.; Pennathur, S.; Kaplan, M.J. Lupus high-density lipoprotein induces proinflammatory responses in macrophages by binding lectin-like oxidised low-density lipoprotein receptor 1 and failing to promote activating transcription factor 3 activity. Ann. Rheum. Dis., 2017, 76(3), 602-611.
[192]
Gaál, K.; Tarr, T.; Lőrincz, H.; Borbás, V.; Seres, I.; Harangi, M.; Fülöp, P.; Paragh, G. High-density lipopoprotein antioxidant capacity, subpopulation distribution and paraoxonase-1 activity in patients with systemic lupus erythematosus. Lipids Health Dis., 2016, 15, 60.
[193]
Shao, B.; Oda, M.N.; Bergt, C.; Fu, X.; Green, P.S.; Brot, N.; Oram, J.F.; Heinecke, J.W. Myeloperoxidase impairs ABCA1-dependent cholesterol efflux through methionine oxidation and site-specific tyrosine chlorination of apolipoprotein A-I. J. Biol. Chem., 2006, 281(14), 9001-9004.
[194]
Pirillo, A.; Uboldi, P.; Kuhn, H.; Catapano, A.L. 15-Lipoxygenase-mediated modification of high-density lipoproteins impairs SR-BI- and ABCA1-dependent cholesterol efflux from macrophages. Biochim. Biophys. Acta, 2006, 1761(3), 292-300.
[195]
Pirillo, A.; Uboldi, P.; Catapano, A.L. Dual effect of hypochlorite in the modification of high density lipoproteins. Biochem. Biophys. Res. Commun., 2010, 403(3-4), 447-451.
[196]
Hafiane, A.; Jabor, B.; Ruel, I.; Ling, J.; Genest, J. High-density lipoprotein mediated cellular cholesterol efflux in acute coronary syndromes. Am. J. Cardiol., 2014, 113(2), 249-255.
[197]
Bellanger, N.; Orsoni, A.; Julia, Z.; Fournier, N.; Frisdal, E.; Duchene, E.; Bruckert, E.; Carrie, A.; Bonnefont-Rousselot, D.; Pirault, J.; Saint-Charles, F.; Chapman, M.J.; Lesnik, P.; Le Goff, W.; Guerin, M. Atheroprotective reverse cholesterol transport pathway is defective in familial hypercholesterolemia. Arterioscler. Thromb. Vasc. Biol., 2011, 31(7), 1675-1681.
[198]
Shiu, S.W.; Wong, Y.; Tan, K.C. Pre-β1 HDL in type 2 diabetes mellitus. Atheroscler., 2017, 263, 24-28.
[199]
Vaisar, T.; Pennathur, S.; Green, P.S.; Gharib, S.A.; Hoofnagle, A.N.; Cheung, M.C.; Byun, J.; Vuletic, S.; Kassim, S.; Singh, P.; Chea, H.; Knopp, R.H.; Brunzell, J.; Geary, R.; Chait, A.; Zhao, X.Q.; Elkon, K.; Marcovina, S.; Ridker, P.; Oram, J.F.; Heinecke, J.W. Shotgun proteomics implicates protease inhibition and complement activation in the antiinflammatory properties of HDL. J. Clin. Invest., 2007, 117(3), 746-756.
[200]
Patel, P.J.; Khera, A.V.; Wilensky, R.L.; Rader, D.J. Anti-oxidative and cholesterol efflux capacities of high-density lipoprotein are reduced in ischaemic cardiomyopathy. Eur. J. Heart Fail., 2013, 15(11), 1215-1219.
[201]
Hussein, H.; Saheb, S.; Couturier, M.; Atassi, M.; Orsoni, A.; Carrié, A.; Therond, P.; Chantepie, S.; Robillard, P.; Bruckert, E.; Chapman, M.J.; Kontush, A. Small, dense high-density lipoprotein 3 particles exhibit defective antioxidative and anti-inflammatory function in familial hypercholesterolemia: Partial correction by low-density lipoprotein apheresis. J. Clin. Lipidol., 2016, 10(1), 124-133.
[202]
Cutuli, L.; Pirillo, A.; Uboldi, P.; Kuehn, H.; Catapano, A.L. 15-lipoxygenase-mediated modification of HDL3 impairs eNOS activation in human endothelial cells. Lipids, 2014, 49(4), 317-326.
[203]
Denimal, D.; Monier, S.; Brindisi, M.C.; Petit, J.M.; Bouillet, B.; Nguyen, A.; Demizieux, L.; Simoneau, I.; Pais de Barros, J.P.; Vergès, B.; Duvillard, L. Impairment of the Ability of HDL From Patients With Metabolic Syndrome but Without Diabetes Mellitus to Activate eNOS: Correction by S1P Enrichment. Arterioscler. Thromb. Vasc. Biol., 2017, 37(5), 804-811.
[204]
Marsche, G.; Heller, R.; Fauler, G.; Kovacevic, A.; Nuszkowski, A.; Graier, W.; Sattler, W.; Malle, E. 2-chlorohexadecanal derived from hypochlorite-modified high-density lipoprotein-associated plasmalogen is a natural inhibitor of endothelial nitric oxide biosynthesis. Arterioscler. Thromb. Vasc. Biol., 2004, 24(12), 2302-2306.
[205]
Jensen, M.K.; Rimm, E.B.; Furtado, J.D.; Sacks, F.M. Apolipoprotein C-III as a potential modulator of the association between HDL-cholesterol and incident coronary heart disease. J. Am. Heart Assoc., 2012, 1(2), jah3-e000232.
[206]
de Souza, J.A.; Vindis, C.; Hansel, B.; Nègre-Salvayre, A.; Therond, P.; Serrano, C.V., Jr; Chantepie, S.; Salvayre, R.; Bruckert, E.; Chapman, M.J.; Kontush, A. Metabolic syndrome features small, apolipoprotein A-I-poor, triglyceride-rich HDL3 particles with defective anti-apoptotic activity. Atheroscler., 2008, 197(1), 84-94.
[207]
Annema, W.; von Eckardstein, A. Dysfunctional high-density lipoproteins in coronary heart disease: implications for diagnostics and therapy. Transl. Res., 2016, 173, 30-57.
[208]
Sorrentino, S.A.; Besler, C.; Rohrer, L.; Meyer, M.; Heinrich, K.; Bahlmann, F.H.; Mueller, M.; Horváth, T.; Doerries, C.; Heinemann, M.; Flemmer, S.; Markowski, A.; Manes, C.; Bahr, M.J.; Haller, H.; von Eckardstein, A.; Drexler, H.; Landmesser, U. Endothelial-vasoprotective effects of high-density lipoprotein are impaired in patients with type 2 diabetes mellitus but are improved after extended-release niacin therapy. Circulation, 2010, 121(1), 110-122.
[209]
Zewinger, S.; Speer, T.; Kleber, M.E.; Scharnagl, H.; Woitas, R.; Lepper, P.M.; Pfahler, K.; Seiler, S.; Heine, G.H.; März, W.; Silbernagel, G.; Fliser, D. HDL cholesterol is not associated with lower mortality in patients with kidney dysfunction. J. Am. Soc. Nephrol., 2014, 25(5), 1073-1082.
[210]
Fogelman, A.M. When good cholesterol goes bad. Nat. Med., 2004, 10(9), 902-903.
[211]
Navab, M.; Yu, R.; Gharavi, N.; Huang, W.; Ezra, N.; Lotfizadeh, A.; Anantharamaiah, G.M.; Alipour, N.; Van Lenten, B.J.; Reddy, S.T.; Marelli, D. High-density lipoprotein: antioxidant and anti-inflammatory properties. Curr. Atheroscler. Rep., 2007, 9(3), 244-248.
[212]
Ansell, B.J.; Navab, M.; Hama, S.; Kamranpour, N.; Fonarow, G.; Hough, G.; Rahmani, S.; Mottahedeh, R.; Dave, R.; Reddy, S.T.; Fogelman, A.M. Inflammatory/antiinflammatory properties of high-density lipoprotein distinguish patients from control subjects better than high-density lipoprotein cholesterol levels and are favorably affected by simvastatin treatment. Circulation, 2003, 108(22), 2751-2756.
[213]
Alwaili, K.; Bailey, D.; Awan, Z.; Bailey, S.D.; Ruel, I.; Hafiane, A.; Krimbou, L.; Laboissiere, S.; Genest, J. The HDL proteome in acute coronary syndromes shifts to an inflammatory profile. Biochim. Biophys. Acta, 2012, 1821(3), 405-415.
[214]
Vaisar, T.; Mayer, P.; Nilsson, E.; Zhao, X.Q.; Knopp, R.; Prazen, B.J. HDL in humans with cardiovascular disease exhibits a proteomic signature. Clin. Chim. Acta, 2010, 411(13-14), 972-979.
[215]
Drexel, H.; Amann, F.W.; Rentsch, K.; Neuenschwander, C.; Luethy, A.; Khan, S.I.; Follath, F. Relation of the level of high-density lipoprotein subfractions to the presence and extent of coronary artery disease. Am. J. Cardiol., 1992, 70(4), 436-440.
[216]
Ganjali, S.; Momtazi, A.A.; Banach, M.; Kovanen, P.T.; Stein, E.A.; Sahebkar, A. HDL abnormalities in familial hypercholesterolemia: Focus on biological functions. Prog. Lipid Res., 2017, 67, 16-26.
[217]
Ottestad, I.O.; Halvorsen, B.; Balstad, T.R.; Otterdal, K.; Borge, G.I.; Brosstad, F.; Myhre, A.M.; Ose, L.; Nenseter, M.S.; Holven, K.B. Triglyceride-rich HDL3 from patients with familial hypercholesterolemia are less able to inhibit cytokine release or to promote cholesterol efflux. J. Nutr., 2006, 136(4), 877-881.
[218]
Hammadah, M.; Kalogeropoulos, A.P.; Georgiopoulou, V.V.; Weber, M.; Wu, Y.; Hazen, S.L.; Butler, J.; Tang, W.H.W. High-density lipoprotein-associated paraoxonase-1 activity for prediction of adverse outcomes in outpatients with chronic heart failure. Eur. J. Heart Fail., 2017, 19(6), 748-755.
[219]
Tang, W.H.; Wu, Y.; Mann, S.; Pepoy, M.; Shrestha, K.; Borowski, A.G.; Hazen, S.L. Diminished antioxidant activity of high-density lipoprotein-associated proteins in systolic heart failure. Circ Heart Fail, 2011, 4(1), 59-64.
[220]
Distelmaier, K.; Wiesbauer, F.; Blessberger, H.; Oravec, S.; Schrutka, L.; Binder, C.; Dostal, E.; Schillinger, M.; Wojta, J.; Lang, I.M.; Maurer, G.; Huber, K.; Goliasch, G. Impaired antioxidant HDL function is associated with premature myocardial infarction. Eur. J. Clin. Invest., 2015, 45(7), 731-738.
[221]
Xiao, C.; Dash, S.; Morgantini, C.; Hegele, R.A.; Lewis, G.F. Pharmacological targeting of the atherogenic dyslipidemia complex: the next frontier in CVD prevention beyond lowering LDL cholesterol. Diabetes, 2016, 65(7), 1767-1778.
[222]
Estruch, M.; Miñambres, I.; Sanchez-Quesada, J.L.; Soler, M.; Pérez, A.; Ordoñez-Llanos, J.; Benitez, S. Increased inflammatory effect of electronegative LDL and decreased protection by HDL in type 2 diabetic patients. Atheroscler., 2017, 265, 292-298.
[223]
Harper, C.R.; Jacobson, T.A. Managing dyslipidemia in chronic kidney disease. J. Am. Coll. Cardiol., 2008, 51(25), 2375-2384.
[224]
Vaziri, N.D. HDL abnormalities in nephrotic syndrome and chronic kidney disease. Nat. Rev. Nephrol., 2016, 12(1), 37-47.
[225]
Speer, T.; Rohrer, L.; Blyszczuk, P.; Shroff, R.; Kuschnerus, K.; Kränkel, N.; Kania, G.; Zewinger, S.; Akhmedov, A.; Shi, Y.; Martin, T.; Perisa, D.; Winnik, S.; Müller, M.F.; Sester, U.; Wernicke, G.; Jung, A.; Gutteck, U.; Eriksson, U.; Geisel, J.; Deanfield, J.; von Eckardstein, A.; Lüscher, T.F.; Fliser, D.; Bahlmann, F.H.; Landmesser, U. Abnormal high-density lipoprotein induces endothelial dysfunction via activation of Toll-like receptor-2. Immunity, 2013, 38(4), 754-768.
[226]
Baragetti, A.; Norata, G.D.; Sarcina, C.; Rastelli, F.; Grigore, L.; Garlaschelli, K.; Uboldi, P.; Baragetti, I.; Pozzi, C.; Catapano, A.L. High density lipoprotein cholesterol levels are an independent predictor of the progression of chronic kidney disease. J. Intern. Med., 2013, 274(3), 252-262.
[227]
Honda, H.; Hirano, T.; Ueda, M.; Kojima, S.; Mashiba, S.; Hayase, Y.; Michihata, T.; Shibata, T. High-density lipoprotein subfractions and their oxidized subfraction particles in patients with chronic kidney disease. J. Atheroscler. Thromb., 2016, 23(1), 81-94.
[228]
Honda, H.; Ueda, M.; Kojima, S.; Mashiba, S.; Michihata, T.; Takahashi, K.; Shishido, K.; Akizawa, T. Oxidized high-density lipoprotein as a risk factor for cardiovascular events in prevalent hemodialysis patients. Atheroscler., 2012, 220(2), 493-501.
[229]
Yamamoto, S.; Yancey, P.G.; Ikizler, T.A.; Jerome, W.G.; Kaseda, R.; Cox, B.; Bian, A.; Shintani, A.; Fogo, A.B.; Linton, M.F.; Fazio, S.; Kon, V. Dysfunctional high-density lipoprotein in patients on chronic hemodialysis. J. Am. Coll. Cardiol., 2012, 60(23), 2372-2379.
[230]
Kalantar-Zadeh, K.; Kopple, J.D.; Kamranpour, N.; Fogelman, A.M.; Navab, M. HDL-inflammatory index correlates with poor outcome in hemodialysis patients. Kidney Int., 2007, 72(9), 1149-1156.
[231]
Shimizu, T.; Tanigawa, H.; Miura, S.; Kuwano, T.; Takata, K.; Suematsu, Y.; Imaizumi, S.; Yahiro, E.; Zhang, B.; Uehara, Y.; Saku, K. Newly developed apolipoprotein A-I mimetic peptide promotes macrophage reverse cholesterol transport in vivo. Int. J. Cardiol., 2015, 192, 82-88.
[232]
Nguyen, S.D.; Javanainen, M.; Rissanen, S.; Zhao, H.; Huusko, J.; Kivelä, A.M.; Ylä-Herttuala, S.; Navab, M.; Fogelman, A.M.; Vattulainen, I.; Kovanen, P.T.; Öörni, K. Apolipoprotein A-I mimetic peptide 4F blocks sphingomyelinase-induced LDL aggregation. J. Lipid Res., 2015, 56(6), 1206-1221.
[233]
Uehara, Y.; Ando, S.; Yahiro, E.; Oniki, K.; Ayaori, M.; Abe, S.; Kawachi, E.; Zhang, B.; Shioi, S.; Tanigawa, H.; Imaizumi, S.; Miura, S.; Saku, K. FAMP, a novel apoA-I mimetic peptide, suppresses aortic plaque formation through promotion of biological HDL function in ApoE-deficient mice. J. Am. Heart Assoc., 2013, 2(3), e000048.
[234]
Amar, M.J.; D’Souza, W.; Turner, S.; Demosky, S.; Sviridov, D.; Stonik, J.; Luchoomun, J.; Voogt, J.; Hellerstein, M.; Sviridov, D.; Remaley, A.T. 5A apolipoprotein mimetic peptide promotes cholesterol efflux and reduces atherosclerosis in mice. J. Pharmacol. Exp. Ther., 2010, 334(2), 634-641.
[235]
Iwata, A.; Miura, S.; Zhang, B.; Imaizumi, S.; Uehara, Y.; Shiomi, M.; Saku, K. Antiatherogenic effects of newly developed apolipoprotein A-I mimetic peptide/phospholipid complexes against aortic plaque burden in Watanabe-heritable hyperlipidemic rabbits. Atheroscler., 2011, 218(2), 300-307.
[236]
Morgantini, C.; Imaizumi, S.; Grijalva, V.; Navab, M.; Fogelman, A.M.; Reddy, S.T. Apolipoprotein A-I mimetic peptides prevent atherosclerosis development and reduce plaque inflammation in a murine model of diabetes. Diabetes, 2010, 59(12), 3223-3228.
[237]
Vecoli, C.; Cao, J.; Neglia, D.; Inoue, K.; Sodhi, K.; Vanella, L.; Gabrielson, K.K.; Bedja, D.; Paolocci, N.; L’abbate, A.; Abraham, N.G. Apolipoprotein A-I mimetic peptide L-4F prevents myocardial and coronary dysfunction in diabetic mice. J. Cell. Biochem., 2011, 112(9), 2616-2626.
[238]
Khera, A.V.; Demler, O.V.; Adelman, S.J.; Collins, H.L.; Glynn, R.J.; Ridker, P.M.; Rader, D.J.; Mora, S. Cholesterol efflux capacity, high-density lipoprotein particle number, and incident cardiovascular events: an analysis from the JUPITER trial (justification for the use of statins in prevention: an intervention trial evaluating rosuvastatin). Circulation, 2017, 135(25), 2494-2504.
[239]
Kim, J.B.; Hama, S.; Hough, G.; Navab, M.; Fogelman, A.M.; Maclellan, W.R.; Horwich, T.B.; Fonarow, G.C. Heart failure is associated with impaired anti-inflammatory and antioxidant properties of high-density lipoproteins. Am. J. Cardiol., 2013, 112(11), 1770-1777.
[240]
Hansel, B.; Giral, P.; Nobecourt, E.; Chantepie, S.; Bruckert, E.; Chapman, M.J.; Kontush, A. Metabolic syndrome is associated with elevated oxidative stress and dysfunctional dense high-density lipoprotein particles displaying impaired antioxidative activity. J. Clin. Endocrinol. Metab., 2004, 89(10), 4963-4971.

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