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Current Medicinal Chemistry

Editor-in-Chief

ISSN (Print): 0929-8673
ISSN (Online): 1875-533X

Review Article

Lipoproteins in Atherosclerosis Process

Author(s): Valentina Arnao, Antonino Tuttolomondo*, Mario Daidone and Antonio Pinto

Volume 26, Issue 9, 2019

Page: [1525 - 1543] Pages: 19

DOI: 10.2174/0929867326666190516103953

Price: $65

Abstract

Background: Dyslipidaemias is a recognized risk factor for atherosclerosis, however, new evidence brought to light by trials investigating therapies to enhance HDLcholesterol have suggested an increased atherosclerotic risk when HDL-C is high.

Results: Several studies highlight the central role in atherosclerotic disease of dysfunctional lipoproteins; oxidised LDL-cholesterol is an important feature, according to “oxidation hypothesis”, of atherosclerotic lesion, however, there is today a growing interest for dysfunctional HDL-cholesterol. The target of our paper is to review the functions of modified and dysfunctional lipoproteins in atherogenesis.

Conclusion: Taking into account the central role recognized to dysfunctional lipoproteins, measurements of functional features of lipoproteins, instead of conventional routine serum evaluation of lipoproteins, could offer a valid contribution in experimental studies as in clinical practice to stratify atherosclerotic risk.

Keywords: Lipoproteins, oxidised, dysfunctional, atherogenisis, dyslipidemia, HDL-C, atherosclerosis.

[1]
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.
[2]
Barter, P.; Kastelein, J.; Nunn, A.; Hobbs, R. High density lipoproteins (HDLs) and atherosclerosis; the unanswered questions. Atherosclerosis, 2003, 168(2), 195-211.
[3]
Maron, D.J.; Fazio, S.; Linton, M.F. Current perspectives on statins. Circulation, 2000, 101(2), 207-213.
[4]
Barquera, S.; Pedroza-Tobías, A.; Medina, C.; Hernández-Barrera, L.; Bibbins-Domingo, K.; Lozano, R.; Moran, A.E. Global overview of the epidemiology of atherosclerotic cardiovascular disease. Arch. Med. Res., 2015, 46(5), 328-338.
[5]
Di Raimondo, D.; Miceli, G.; Musiari, G.; Tuttolomondo, A.; Pinto, A. New insights about the putative role of myokines in the context of cardiac rehabilitation and secondary cardiovascular prevention. Ann. Transl. Med., 2017, 5(15), 300.
[6]
Di Raimondo, D.; Musiari, G.; Miceli, G.; Arnao, V.; Pinto, A. Preventive and therapeutic role of muscle contraction against chronic diseases. Curr. Pharm. Des., 2016, 22(30), 4686-4699.
[7]
Di Raimondo, D.; Tuttolomondo, A.; Musiari, G.; Schimmenti, C.; D’Angelo, A.; Pinto, A. Are the myokines the mediators of physical activity-induced health benefits? Curr. Pharm. Des., 2016, 22(24), 3622-3647.
[8]
Di Raimondo, D.; Tuttolomondo, A.; Buttà, C.; Casuccio, A.; Giarrusso, L.; Miceli, G.; Licata, G.; Pinto, A. Metabolic and anti-inflammatory effects of a home-based programme of aerobic physical exercise. Int. J. Clin. Pract., 2013, 67(12), 1247-1253.
[9]
Anderson, K.M.; Castelli, W.P.; Levy, D. Cholesterol and mortality. 30 years of follow-up from the Framingham study. JAMA, 1987, 257(16), 2176-2180.
[10]
Martin, M.J.; Hulley, S.B.; Browner, W.S.; Kuller, L.H.; Wentworth, D. Serum cholesterol, blood pressure, and mortality: implications from a cohort of 361,662 men. Lancet, 1986, 2(8513), 933-936.
[11]
Tsimikas, S.; Brilakis, E.S.; Miller, E.R.; McConnell, J.P.; Lennon, R.J.; Kornman, K.S.; Witztum, J.L.; Berger, P.B. Oxidized phospholipids, Lp(a) lipoprotein, and coronary artery disease. N. Engl. J. Med., 2005, 353(1), 46-57.
[12]
Roger, V.L.; Go, A.S.; Lloyd-Jones, D.M.; Benjamin, E.J.; Berry, J.D.; Borden, W.B.; Bravata, D.M.; Dai, S.; Ford, E.S.; Fox, C.S.; Fullerton, H.J.; Gillespie, C.; Hailpern, S.M.; Heit, J.A.; Howard, V.J.; Kissela, B.M.; Kittner, S.J.; Lackland, D.T.; Lichtman, J.H.; Lisabeth, L.D.; Makuc, D.M.; Marcus, G.M.; Marelli, A.; Matchar, D.B.; Moy, C.S.; Mozaffarian, D.; Mussolino, M.E.; Nichol, G.; Paynter, N.P.; Soliman, E.Z.; Sorlie, P.D.; Sotoodehnia, N.; Turan, T.N.; Virani, S.S.; Wong, N.D.; Woo, D.; Turner, M.B. American heart association statistics committee and stroke statistics subcommittee. heart disease and stroke statistics--2012 update: a report from the american heart association. Circulation, 2012, 125(1), e2-e220.
[13]
Libby, P. Inflammation in atherosclerosis. Nature, 2002, 420(6917), 868-874.
[14]
Roger, V.L.; Go, A.S.; Lloyd-Jones, D.M.; Adams, R.J.; Berry, J.D.; Brown, T.M.; Carnethon, M.R.; Dai, S.; de Simone, G.; Ford, E.S.; Fox, C.S.; Fullerton, H.J.; Gillespie, C.; Greenlund, K.J.; Hailpern, S.M.; Heit, J.A.; Ho, P.M.; Howard, V.J.; Kissela, B.M.; Kittner, S.J.; Lackland, D.T.; Lichtman, J.H.; Lisabeth, L.D.; Makuc, D.M.; Marcus, G.M.; Marelli, A.; Matchar, D.B.; McDermott, M.M.; Meigs, J.B.; Moy, C.S.; Mozaffarian, D.; Mussolino, M.E.; Nichol, G.; Paynter, N.P.; Rosamond, W.D.; Sorlie, P.D.; Stafford, R.S.; Turan, T.N.; Turner, M.B.; Wong, N.D.; Wylie-Rosett, J. American heart association statistics committee and stroke statistics subcommittee. Heart disease and stroke statistics--2011 update: a report from the American heart association. Circulation, 2011, 123(4), e18-e209.
[15]
Centers for Disease Control and Prevention (CDC). State-specific cholesterol screening trends: United States, 1991–1999. MMWR Morb. Mortal. Wkly. Rep., 2001, 50(35), 754-758.
[16]
Zhang, L.; Qiao, Q.; Tuomilehto, J.; Hammar, N.; Ruotolo, G.; Stehouwer, C.D.; Heine, R.J.; Eliasson, M.; Zethelius, B. DECODE Study Group. The impact of dyslipidaemia on cardiovascular mortality in individuals without a prior history of diabetes in the DECODE Study. Atherosclerosis, 2009, 206(1), 298-302.
[17]
Fodor, J.G.; Frohlich, J.J.; Genest, J.J.G., Jr; McPherson, P.R. Recommendations for the management and treatment of dyslipidemia. CMAJ, 2000, 162(10), 1441-1447.
[18]
Stancu, C.S.; Toma, L.; Sima, A.V. Dual role of lipoproteins in endothelial cell dysfunction in atherosclerosis. Cell Tissue Res., 2012, 349(2), 433-446.
[19]
Mayes, P.A. Cholesterol synthesis, transport, and excretion. Harper’s Biochem 23., 1993, 266-278.
[20]
Johansson, J.; Carlson, L.A.; Landou, C.; Hamsten, A. High density lipoproteins and coronary atherosclerosis. A strong inverse relation with the largest particles is confined to normotriglyceridemic patients. Arterioscler. Thromb., 1991, 11(1), 174-182.
[21]
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.
[22]
El Harchaoui, K.; Arsenault, B.J.; Franssen, R.; Després, J.P.; Hovingh, G.K.; Stroes, E.S.G.; Otvos, J.D.; Wareham, N.J.; Kastelein, J.J.; Khaw, K.T.; Boekholdt, S.M. High-density lipoprotein particle size and concentration and coronary risk. Ann. Intern. Med., 2009, 150(2), 84-93.
[23]
Champe, P.C.; Harvey, R.A. Cholesterol and steroid metabolism. Lippincott’s illustrated reviews. Biochem 2., 1994, 205-228.
[24]
Marinetti, G. V. Dietary management of elevated blood lipids. Disorders of lipid metabolism., 1990, 135-168.
[25]
Attie, A.D.; Kastelein, J.P.; Hayden, M.R. Pivotal role of ABCA1 in reverse cholesterol transport influencing HDL levels and susceptibility to atherosclerosis. J. Lipid Res., 2001, 42(11), 1717-1726.
[26]
Ansell, B.J.; Fonarow, G.C.; Fogelman, A.M. The paradox of dysfunctional high-density lipoprotein. Curr. Opin. Lipidol., 2007, 18(4), 427-434.
[27]
Bermúdez, V.; Cano, R.; Cano, C.; Bermúdez, F.; Arraiz, N.; Acosta, L.; Finol, F.; Pabón, M.R.; Amell, A.; Reyna, N.; Hidalgo, J.; Kendall, P.; Manuel, V.; Hernández, R. Pharmacologic management of isolated low high-density lipoprotein syndrome. Am. J. Ther., 2008, 15(4), 377-388.
[28]
Brousseau, M.E.; Schaefer, E.J.; Wolfe, M.L.; Bloedon, L.T.; Digenio, A.G.; Clark, R.W.; Mancuso, J.P.; Rader, D.J. Effects of an inhibitor of cholesteryl ester transfer protein on HDL cholesterol. N. Engl. J. Med., 2004, 350(15), 1505-1515.
[29]
Kastelein, J.J.; van Leuven, S.I.; Burgess, L.; Evans, G.W.; Kuivenhoven, J.A.; Barter, P.J.; Revkin, J.H.; Grobbee, D.E.; Riley, W.A.; Shear, C.L.; Duggan, W.T.; Bots, M.L. RADIANCE 1 Investigators. Effect of torcetrapib on carotid atherosclerosis in familial hypercholesterolemia. N. Engl. J. Med., 2007, 356(16), 1620-1630.
[30]
Ansell, B.J.; Fonarow, G.C.; Fogelman, A.M. High-density lipoprotein: is it always atheroprotective? Curr. Atheroscler. Rep., 2006, 8(5), 405-411.
[31]
Norata, G.D.; Pirillo, A.; Catapano, A.L. Statins and oxidative stress during atherogenesis. J. Cardiovasc. Risk, 2003, 10(3), 181-189.
[32]
Leeuwenburgh, C.; Hardy, M.M.; Hazen, S.L.; Wagner, P.; Oh-ishi, S.; Steinbrecher, U.P.; Heinecke, J.W. Reactive nitrogen intermediates promote low density lipoprotein oxidation in human atherosclerotic intima. J. Biol. Chem., 1997, 272(3), 1433-1436.
[33]
Lougheed, M.; Steinbrecher, U.P. Mechanism of uptake of copper-oxidized low density lipoprotein in macrophages is dependent on its extent of oxidation. J. Biol. Chem., 1996, 271(20), 11798-11805.
[34]
Navab, M.; Imes, S.S.; Hama, S.Y.; Hough, G.P.; Ross, L.A.; Bork, R.W.; Valente, A.J.; Berliner, J.A.; Drinkwater, D.C.; Laks, H. Monocyte transmigration induced by modification of low density lipoprotein in cocultures of human aortic wall cells is due to induction of monocyte chemotactic protein 1 synthesis and is abolished by high density lipoprotein. J. Clin. Invest., 1991, 88(6), 2039-2046.
[35]
Choi, S.H.; Sviridov, D.; Miller, Y.I. Oxidized cholesteryl esters and inflammation. Biochim. Biophys. Acta Mol. Cell Biol. Lipids, 2017, 1862(4), 393-397.
[36]
Esterbauer, H.; Jürgens, G.; Quehenberger, O.; Koller, E. Autoxidation of human low density lipoprotein: loss of polyunsaturated fatty acids and vitamin E and generation of aldehydes. J. Lipid Res., 1987, 28(5), 495-509.
[37]
Parthasarathy, S.; Steinbrecher, U.P.; Barnett, J.; Witztum, J.L.; Steinberg, D. Essential role of phospholipase A2 activity in endothelial cell-induced modification of low density lipoprotein. Proc. Natl. Acad. Sci. USA, 1985, 82(9), 3000-3004.
[38]
Goldstein, J.L.; Ho, Y.K.; Basu, S.K.; Brown, M.S. Binding site on macrophages that mediates uptake and degradation of acetylated low density lipoprotein, producing massive cholesterol deposition. Proc. Natl. Acad. Sci. USA, 1979, 76(1), 333-337.
[39]
Heinecke, J.W.; Rosen, H.; Chait, A. Iron and copper promote modification of low density lipoprotein by human arterial smooth muscle cells in culture. J. Clin. Invest., 1984, 74(5), 1890-1894.
[40]
Henriksen, T.; Mahoney, E.M.; Steinberg, D. Enhanced macrophage degradation of low density lipoprotein previously incubated with cultured endothelial cells: recognition by receptors for acetylated low density lipoproteins. Proc. Natl. Acad. Sci. USA, 1981, 78(10), 6499-6503.
[41]
Parthasarathy, S.; Printz, D.J.; Boyd, D.; Joy, L.; Steinberg, D. Macrophage oxidation of low density lipoprotein generates a modified form recognized by the scavenger receptor. Arteriosclerosis, 1986, 6(5), 505-510.
[42]
Liao, J.K.; Shin, W.S.; Lee, W.Y.; Clark, S.L. Oxidized low-density lipoprotein decreases the expression of endothelial nitric oxide synthase. J. Biol. Chem., 1995, 270(1), 319-324.
[43]
Kugiyama, K.; Kerns, S.A.; Morrisett, J.D.; Roberts, R.; Henry, P.D. Impairment of endothelium-dependent arterial relaxation by lysolecithin in modified low-density lipoproteins. Nature, 1990, 344(6262), 160-162.
[44]
Witztum, J.L.; Steinberg, D. Role of oxidized low density lipoprotein in atherogenesis. J. Clin. Invest., 1991, 88(6), 1785-1792.
[45]
Murohara, T.; Kugiyama, K.; Ohgushi, M.; Sugiyama, S.; Ohta, Y.; Yasue, H. LPC in oxidized LDL elicits vasocontraction and inhibits endothelium- dependent relaxation. Am. J. Physiol., 1994, 267(6 Pt 2), H2441-H2449.
[46]
Quinn, M.T.; Parthasarathy, S.; Steinberg, D. Lysophosphatidylcholine: a chemotactic factor for human monocytes and its potential role in atherogenesis. Proc. Natl. Acad. Sci. USA, 1988, 85(8), 2805-2809.
[47]
Aviram, M. Modified forms of low density lipoprotein affect platelet aggregation in vitro. Thromb. Res., 1989, 53(6), 561-567.
[48]
Kugiyama, K.; Sakamoto, T.; Misumi, I.; Sugiyama, S.; Ohgushi, M.; Ogawa, H.; Horiguchi, M.; Yasue, H. Transferable lipids in oxidized low-density lipoprotein stimulate plasminogen activator inhibitor-1 and inhibit tissue-type plasminogen activator release from endothelial cells. Circ. Res., 1993, 73(2), 335-343.
[49]
White, D. A. The phospholipid composition in mammalian tissues. Form and function of phospholipids, 1973, 441- 482.
[50]
Liu, S-Y.; Lu, X.; Choy, S.; Dembinski, T.C.; Hatch, G.M.; Mymin, D.; Shen, X.; Angel, A.; Choy, P.C.; Man, R.Y.K. Alteration of lysophosphatidylcholine content in low density lipoprotein after oxidative modification: relationship to endothelium dependent relaxation. Cardiovasc. Res., 1994, 28(10), 1476-1481.
[51]
Yokoyama, M.; Hirata, K.; Miyake, R.; Akita, H.; Ishikawa, Y.; Fukuzaki, H. Lysophosphatidylcholine: essential role in the inhibition of endothelium-dependent vasorelaxation by oxidized low density lipoprotein. Biochem. Biophys. Res. Commun., 1990, 168(1), 301-308.
[52]
Simon, B.C.; Cunningham, L.D.; Cohen, R.A. Oxidized low density lipoproteins cause contraction and inhibit endothelium-dependent relaxation in the pig coronary artery. J. Clin. Invest., 1990, 86(1), 75-79.
[53]
Hirata, K.; Miki, N.; Kuroda, Y.; Sakoda, T.; Kawashima, S.; Yokoyama, M. Low concentration of oxidized low-density lipoprotein and lysophosphatidylcholine upregulate constitutive nitric oxide synthase mRNA expression in bovine aortic endothelial cells. Circ. Res., 1995, 76(6), 958-962.
[54]
Choy, P.C.; Siow, Y.L.; Mymin, D. O, K. Lipids and atherosclerosis. Biochem. Cell Biol., 2004, 82(1), 212-224.
[55]
Calabresi, L.; Gomaraschi, M.; Franceschini, G. Endothelial protection by high-density lipoproteins: from bench to bedside. Arterioscler. Thromb. Vasc. Biol., 2003, 23(10), 1724-1731.
[56]
Norata, G.D.; Catapano, A.L. Molecular mechanisms responsible for the antiinflammatory and protective effect of HDL on the endothelium. Vasc. Health Risk Manag., 2005, 1(2), 119-129.
[57]
Nofer, J.R.; Kehrel, B.; Fobker, M.; Levkau, B.; Assmann, G.; von Eckardstein, A. HDL and arteriosclerosis: beyond reverse cholesterol transport. Atherosclerosis, 2002, 161(1), 1-16.
[58]
Norata, G.D.; Pirillo, A.; Catapano, A.L. Modified HDL: biological and physiopathological consequences. Nutr. Metab. Cardiovasc. Dis., 2006, 16(5), 371-386.
[59]
Navab, M.; Hama, S.Y.; Hough, G.P.; Subbanagounder, G.; Reddy, S.T.; Fogelman, A.M. A cell-free assay for detecting HDL that is dysfunctional in preventing the formation of or inactivating oxidized phospholipids. J. Lipid Res., 2001, 42(8), 1308-1317.
[60]
Bérard, A.M.; Föger, B.; Remaley, A.; Shamburek, R.; Vaisman, B.L.; Talley, G.; Paigen, B.; Hoyt, R.F., Jr; Marcovina, S.; Brewer, H.B., Jr; Santamarina-Fojo, S. High plasma HDL concentrations associated with enhanced atherosclerosis in transgenic mice overexpressing lecithin-cholesteryl acyltransferase. Nat. Med., 1997, 3(7), 744-749.
[61]
Link, J.J.; Rohatgi, A.; de Lemos, J.A. HDL cholesterol: physiology, pathophysiology, and management. Curr. Probl. Cardiol., 2007, 32(5), 268-314.
[62]
Navab, M.; Hama, S.Y.; Cooke, C.J.; Anantharamaiah, G.M.; Chaddha, M.; Jin, L.; Subbanagounder, G.; Faull, K.F.; Reddy, S.T.; Miller, N.E.; Fogelman, A.M. Normal high density lipoprotein inhibits three steps in the formation of mildly oxidized low density lipoprotein: step 1. J. Lipid Res., 2000, 41(9), 1481-1494.
[63]
Navab, M.; Ananthramaiah, G.M.; Reddy, S.T.; Van Lenten, B.J.; Ansell, B.J.; Fonarow, G.C.; Vahabzadeh, K.; Hama, S.; Hough, G.; Kamranpour, N.; Berliner, J.A.; Lusis, A.J.; Fogelman, A.M. The oxidation hypothesis of atherogenesis: the role of oxidized phospholipids and HDL. J. Lipid Res., 2004, 45(6), 993-1007.
[64]
Navab, M.; Hama, S.Y.; Anantharamaiah, G.M.; Hassan, K.; Hough, G.P.; Watson, A.D.; Reddy, S.T.; Sevanian, A.; Fonarow, G.C.; Fogelman, A.M. Normal high density lipoprotein inhibits three steps in the formation of mildly oxidized low density lipoprotein: steps 2 and 3. J. Lipid Res., 2000, 41(9), 1495-1508.
[65]
Navab, M.; Berliner, J.A.; Subbanagounder, G.; Hama, S.; Lusis, A.J.; Castellani, L.W.; Reddy, S.; Shih, D.; Shi, W.; Watson, A.D.; Van Lenten, B.J.; Vora, D.; Fogelman, A.M. HDL and the inflammatory response induced by LDL-derived oxidized phospholipids. Arterioscler. Thromb. Vasc. Biol., 2001, 21(4), 481-488.
[66]
Shih, D.M.; Xia, Y.R.; Wang, X.P.; Miller, E.; Castellani, L.W.; Subbanagounder, G.; Cheroutre, H.; Faull, K.F.; Berliner, J.A.; Witztum, J.L.; Lusis, A.J. Combined serum paraoxonase knockout/apolipoprotein E knockout mice exhibit increased lipoprotein oxidation and atherosclerosis. J. Biol. Chem., 2000, 275(23), 17527-17535.
[67]
Tward, A.; Xia, Y.R.; Wang, X.P.; Shi, Y.S.; Park, C.; Castellani, L.W.; Lusis, A.J.; Shih, D.M. Decreased atherosclerotic lesion formation in human serum paraoxonase transgenic mice. Circulation, 2002, 106(4), 484-490.
[68]
Tselepis, A.D.; John Chapman, M. Inflammation, bioactive lipids and atherosclerosis: potential roles of a lipoprotein-associated phospholipase A2, platelet activating factor-acetylhydrolase. Atheroscler. Suppl., 2002, 3(4), 57-68.
[69]
Aviram, M.; Rosenblat, M. Paraoxonases 1, 2, and 3, oxidative stress, and macrophage foam cell formation during atherosclerosis development. Free Radic. Biol. Med., 2004, 37(9), 1304-1316.
[70]
Forte, T.M.; Subbanagounder, G.; Berliner, J.A.; Blanche, P.J.; Clermont, A.O.; Jia, Z.; Oda, M.N.; Krauss, R.M.; Bielicki, J.K. Altered activities of anti-atherogenic enzymes LCAT, paraoxonase, and platelet-activating factor acetylhydrolase in atherosclerosis-susceptible mice. J. Lipid Res., 2002, 43(3), 477-485.
[71]
Negre-Salvayre, A.; Dousset, N.; Ferretti, G.; Bacchetti, T.; Curatola, G.; Salvayre, R. Antioxidant and cytoprotective properties of high-density lipoproteins in vascular cells. Free Radic. Biol. Med., 2006, 41(7), 1031-1040.
[72]
Rosenblat, M.; Vaya, J.; Shih, D.; Aviram, M. Paraoxonase 1 (PON1) enhances HDL-mediated macrophage cholesterol efflux via the ABCA1 transporter in association with increased HDL binding to the cells: a possible role for lysophosphatidylcholine. Atherosclerosis, 2005, 179(1), 69-77.
[73]
Ansell, B.J.; Fonarow, G.C.; Fogelman, A.M. The paradox of dysfunctional high-density lipoprotein. Curr. Opin. Lipidol., 2007, 18(4), 427-434.
[74]
Galle, J.; Ochslen, M.; Schollmeyer, P.; Wanner, C. Oxidized lipoproteins inhibit endothelium-dependent vasodilation. Effects of pressure and high-density lipoprotein. Hypertension, 1994, 23(5), 556-564.
[75]
Navab, M.; Hama, S.Y.; Hough, G.P.; Subbanagounder, G.; Reddy, S.T.; Fogelman, A.M. A cell-free assay for detecting HDL that is dysfunctional in preventing the formation of or inactivating oxidized phospholipids. J. Lipid Res., 2001, 42(8), 1308-1317.
[76]
Watson, A.D.; Navab, M.; Hama, S.Y.; Sevanian, A.; Prescott, S.M.; Stafforini, D.M.; McIntyre, T.M.; Du, B.N.; Fogelman, A.M.; Berliner, J.A. Effect of platelet activating factor-acetylhydrolase on the formation and action of minimally oxidized low density lipoprotein. J. Clin. Invest., 1995, 95(2), 774-782.
[77]
Mackness, M.I.; Arrol, S.; Durrington, P.N. Paraoxonase prevents accumulation of lipoperoxides in low-density lipoprotein. FEBS Lett., 1991, 286(1-2), 152-154.
[78]
Aviram, M.; Rosenblat, M.; Bisgaier, C.L.; Newton, R.S.; Primo-Parmo, S.L.; La Du, B.N. Paraoxonase inhibits high-density lipoprotein oxidation and preserves its functions. A possible peroxidative role for paraoxonase. J. Clin. Invest., 1998, 101(8), 1581-1590.
[79]
Aviram, M.; Hardak, E.; Vaya, J.; Mahmood, S.; Milo, S.; Hoffman, A.; Billicke, S.; Draganov, D.; Rosenblat, M. Human serum paraoxonases (PON1) Q and R selectively decrease lipid peroxides in human coronary and carotid atherosclerotic lesions: PON1 esterase and peroxidase-like activities. Circulation, 2000, 101(21), 2510-2517.
[80]
Shih, D.M.; Xia, Y.R.; Wang, X.P.; Miller, E.; Castellani, L.W.; Subbanagounder, G.; Cheroutre, H.; Faull, K.F.; Berliner, J.A.; Witztum, J.L.; Lusis, A.J. Combined serum paraoxonase knockout/apolipoprotein E knockout mice exhibit increased lipoprotein oxidation and atherosclerosis. J. Biol. Chem., 2000, 275(23), 17527-17535.
[81]
Stafforini, D.M.; Zimmerman, G.A.; McIntyre, T.M.; Prescott, S.M. The platelet-activating factor acetylhydrolase from human plasma prevents oxidative modification of low-density lipoprotein. Trans. Assoc. Am. Physicians, 1992, 105, 44-63.
[82]
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.
[83]
Goyal, J.; Wang, K.; Liu, M.; Subbaiah, P.V. Novel function of lecithin-cholesterol acyltransferase. Hydrolysis of oxidized polar phospholipids generated during lipoprotein oxidation. J. Biol. Chem., 1997, 272(26), 16231-16239.
[84]
Liu, M.; St Clair, R.W.; Subbaiah, P.V. Impaired function of lecithin: cholesterol acyltransferase in atherosclerosis-susceptible White Carneau pigeons: possible effects on metabolism of oxidized phospholipids. J. Lipid Res., 1998, 39(2), 245-254.
[85]
Subramanian, V.S.; Goyal, J.; Miwa, M.; Sugatami, J.; Akiyama, M.; Liu, M.; Subbaiah, P.V. Role of lecithin-cholesterol acyltransferase in the metabolism of oxidized phospholipids in plasma: studies with platelet-activating factor-acetyl hydrolase-deficient plasma. Biochim. Biophys. Acta, 1999, 1439(1), 95-109.
[86]
Vohl, M.C.; Neville, T.A.; Kumarathasan, R.; Braschi, S.; Sparks, D.L. A novel lecithin-cholesterol acyltransferase antioxidant activity prevents the formation of oxidized lipids during lipoprotein oxidation. Biochem., 1999, 38(19), 5976-5981.
[87]
Itabe, H.; Hosoya, R.; Karasawa, K.; Jimi, S.; Saku, K.; Takebayashi, S.; Imanaka, T.; Takano, T. Metabolism of oxidized phosphatidylcholines formed in oxidized low density lipoprotein by lecithin-cholesterol acyltransferase. J. Biochem., 1999, 126(1), 153-161.
[88]
Chen, N.; Liu, Y.; Greiner, C.D.; Holtzman, J.L. Physiologic concentrations of homocysteine inhibit the human plasma GSH peroxidase that reduces organic hydroperoxides. J. Lab. Clin. Med., 2000, 136(1), 58-65.
[89]
Nagano, Y.; Arai, H.; Kita, T. High density lipoprotein loses its effect to stimulate efflux of cholesterol from foam cells after oxidative modification. Proc. Natl. Acad. Sci. USA, 1991, 88(15), 6457-6461.
[90]
Hurtado, I.; Fiol, C.; Gracia, V.; Caldú, P. In vitro oxidised HDL exerts a cytotoxic effect on macrophages. Atherosclerosis, 1996, 125(1), 39-46.
[91]
Nakajima, T.; Origuchi, N.; Matsunaga, T.; Kawai, S.; Hokari, S.; Nakamura, H.; Inoue, I.; Katayama, S.; Nagata, A.; Komoda, T. Localization of oxidized HDL in atheromatous plaques and oxidized HDL binding sites on human aortic endothelial cells. Ann. Clin. Biochem., 2000, 37(Pt 2), 179-186.
[92]
Matsunaga, T.; Hokari, S.; Koyama, I.; Harada, T.; Komoda, T. NF-kappa B activation in endothelial cells treated with oxidized high-density lipoprotein. Biochem. Biophys. Res. Commun., 2003, 303(1), 313-319.
[93]
Daugherty, A.; Dunn, J.L.; Rateri, D.L.; Heinecke, J.W. Myeloperoxidase, a catalyst for lipoprotein oxidation, is expressed in human atherosclerotic lesions. J. Clin. Invest., 1994, 94(1), 437-444.
[94]
Bergt, C.; Reicher, H.; Malle, E.; Sattler, W. Hypochlorite modification of high density lipoprotein: effects on cholesterol efflux from J774 macrophages. FEBS Lett., 1999, 452(3), 295-300.
[95]
Marsche, G.; Hammer, A.; Oskolkova, O.; Kozarsky, K.F.; Sattler, W.; Malle, E. Hypochlorite-modified high density lipoprotein, a high affinity ligand to scavenger receptor class B, type I, impairs high density lipoprotein-dependent selective lipid uptake and reverse cholesterol transport. J. Biol. Chem., 2002, 277(35), 32172-32179.
[96]
Suc, I.; Brunet, S.; Mitchell, G.; Rivard, G.E.; Levy, E. Oxidative tyrosylation of high density lipoproteins impairs cholesterol efflux from mouse J774 macrophages: role of scavenger receptors, classes A and B. J. Cell Sci., 2003, 116(Pt 1), 89-99.
[97]
Lee, M.; Lindstedt, L.K.; Kovanen, P.T. Mast cell-mediated inhibition of reverse cholesterol transport. Arterioscler. Thromb., 1992, 12(11), 1329-1335.
[98]
Lindstedt, L.; Saarinen, J.; Kalkkinen, N.; Welgus, H.; Kovanen, P.T. Matrix metalloproteinases-3, -7, and -12, but not -9, reduce high density lipoprotein-induced cholesterol efflux from human macrophage foam cells by truncation of the carboxyl terminus of apolipoprotein A-I. Parallel losses of pre-beta particles and the high affinity component of efflux. J. Biol. Chem., 1999, 274(32), 22627-22634.
[99]
Pirillo, A.; Ghiselli, G. Enhanced macrophage uptake of elastase-modified high-density lipoproteins. Biochem. Biophys. Res. Commun., 2000, 271(2), 386-391.
[100]
Gauster, M.; Oskolkova, O.V.; Innerlohinger, J.; Glatter, O.; Knipping, G.; Frank, S. Endothelial lipase-modified high-density lipoprotein exhibits diminished ability to mediate SR-BI (scavenger receptor B type I)-dependent free-cholesterol efflux. Biochem. J., 2004, 382(Pt 1), 75-82.
[101]
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.
[102]
Chen, Y.D.; Jeng, C.Y.; Reaven, G.M. HDL metabolism in diabetes. Diabetes Metab. Rev., 1987, 3(3), 653-668.
[103]
Ferretti, G.; Bacchetti, T.; Marchionni, C.; Caldarelli, L.; Curatola, G. Effect of glycation of high density lipoproteins on their physicochemical properties and on paraoxonase activity. Acta Diabetol., 2001, 38(4), 163-169.
[104]
Hedrick, C.C.; Thorpe, S.R.; Fu, M.X.; Harper, C.M.; Yoo, J.; Kim, S.M.; Wong, H.; Peters, A.L. Glycation impairs high-density lipoprotein function. Diabetologia, 2000, 43(3), 312-320.
[105]
Witztum, J.L.; Fisher, M.; Pietro, T.; Steinbrecher, U.P.; Elam, R.L. Nonenzymatic glucosylation of high-density lipoprotein accelerates its catabolism in guinea pigs. Diabetes, 1982, 31(11), 1029-1032.
[106]
Duell, P.B.; Oram, J.F.; Bierman, E.L. Nonenzymatic glycosylation of HDL resulting in inhibition of high-affinity binding to cultured human fibroblasts. Diabetes, 1990, 39(10), 1257-1263.
[107]
Duell, P.B.; Oram, J.F.; Bierman, E.L. Nonenzymatic glycosylation of HDL and impaired HDL-receptor-mediated cholesterol efflux. Diabetes, 1991, 40(3), 377-384.
[108]
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.
[109]
Beg, Z.H.; Stonik, J.A.; Hoeg, J.M.; Demosky, S.J., Jr; Fairwell, T.; Brewer, H.B., Jr Human apolipoprotein A-I. Post-translational modification by covalent phosphorylation. J. Biol. Chem., 1989, 264(12), 6913-6921.
[110]
Hoeg, J.M.; Meng, M.S.; Ronan, R.; Fairwell, T.; Brewer, H.B., Jr Human apolipoprotein A-I. Post-translational modification by fatty acid acylation. J. Biol. Chem., 1986, 261(9), 3911-3914.
[111]
Fernández-Irigoyen, J.; Santamaría, E.; Sesma, L.; Muñoz, J.; Riezu, J.I.; Caballería, J.; Lu, S.C.; Prieto, J.; Mato, J.M.; Avila, M.A.; Corrales, F.J. Oxidation of specific methionine and tryptophan residues of apolipoprotein A-I in hepatocarcinogenesis. Proteomics, 2005, 5(18), 4964-4972.
[112]
Vivanco, F.; Martín-Ventura, J.L.; Duran, M.C.; Barderas, M.G.; Blanco-Colio, L.; Dardé, V.M.; Mas, S.; Meilhac, O.; Michel, J.B.; Tuñón, J.; Egido, J. Quest for novel cardiovascular biomarkers by proteomic analysis. J. Proteome Res., 2005, 4(4), 1181-1191.
[113]
Erqou, S.; Thompson, A.; Di Angelantonio, E.; Saleheen, D.; Kaptoge, S.; Marcovina, S.; Danesh, J. Apolipoprotein(a) isoforms and the risk of vascular disease: systematic review of 40 studies involving 58,000 participants. J. Am. Coll. Cardiol., 2010, 55(19), 2160-2167.
[114]
Erqou, S.; Kaptoge, S.; Perry, P.L.; Di Angelantonio, E.; Thompson, A.; White, I.R.; Marcovina, S.M.; Collins, R.; Thompson, S.G.; Danesh, J. Emerging Risk Factors Collaboration. Lipoprotein(a) concentration and the risk of coronary heart disease, stroke, and nonvascular mortality. JAMA, 2009, 302(4), 412-423.
[115]
Hopewell, J.C.; Seedorf, U.; Farrall, M.; Parish, S.; Kyriakou, T.; Goel, A.; Hamsten, A.; Collins, R.; Watkins, H.; Clarke, R. PROCARDIS Consortium. Impact of lipoprotein(a) levels and apolipoprotein(a) isoform size on risk of coronary heart disease. J. Intern. Med., 2014, 276(3), 260-268.
[116]
Kronenberg, F.; Utermann, G. Lipoprotein(a): resurrected by genetics. J. Intern. Med., 2013, 273(1), 6-30.
[117]
Laschkolnig, A.; Kollerits, B.; Lamina, C.; Meisinger, C.; Rantner, B.; Stadler, M.; Peters, A.; Koenig, W.; Stöckl, A.; Dähnhardt, D.; Böger, C.A.; Krämer, B.K.; Fraedrich, G.; Strauch, K.; Kronenberg, F. Lipoprotein (a) concentrations, apolipoprotein (a) phenotypes, and peripheral arterial disease in three independent cohorts. Cardiovasc. Res., 2014, 103(1), 28-36.
[118]
Kamstrup, P.R.; Tybjærg-Hansen, A.; Nordestgaard, B.G. Elevated lipoprotein(a) and risk of aortic valve stenosis in the general population. J. Am. Coll. Cardiol., 2014, 63(5), 470-477.
[119]
Capoulade, R.; Chan, K.L.; Yeang, C.; Mathieu, P.; Bossé, Y.; Dumesnil, J.G.; Tam, J.W.; Teo, K.K.; Mahmut, A.; Yang, X.; Witztum, J.L.; Arsenault, B.J.; Després, J.P.; Pibarot, P.; Tsimikas, S. Oxidized phospholipids, lipoprotein(a), and progression of calcific aortic valve stenosis. J. Am. Coll. Cardiol., 2015, 66(11), 1236-1246.
[120]
Koschinsky, M.L.; Boffa, M.B. Lipoprotein(a): an important cardiovascular risk factor and a clinical conundrum. Endocrinol. Metab. Clin. North Am., 2014, 43(4), 949-962.
[121]
Kelly, E.; Hemphill, L. Lipoprotein(a): A lipoprotein whose time has come. Curr. Treat. Options Cardiovasc. Med., 2017, 19(7), 48.
[122]
Tsimikas, S.; Brilakis, E.S.; Miller, E.R.; McConnell, J.P.; Lennon, R.J.; Kornman, K.S.; Witztum, J.L.; Berger, P.B. Oxidized phospholipids, Lp(a) lipoprotein, and coronary artery disease. N. Engl. J. Med., 2005, 353(1), 46-57.
[123]
Bergmark, C.; Dewan, A.; Orsoni, A.; Merki, E.; Miller, E.R.; Shin, M.J.; Binder, C.J.; Hörkkö, S.; Krauss, R.M.; Chapman, M.J.; Witztum, J.L.; Tsimikas, S. A novel function of lipoprotein [a] as a preferential carrier of oxidized phospholipids in human plasma. J. Lipid Res., 2008, 49(10), 2230-2239.
[124]
Marcovina, S.M.; Koschinsky, M.L. Evaluation of lipoprotein(a) as a prothrombotic factor: progress from bench to bedside. Curr. Opin. Lipidol., 2003, 14(4), 361-366.
[125]
Viney, N.J.; van Capelleveen, J.C.; Geary, R.S.; Xia, S.; Tami, J.A.; Yu, R.Z.; Marcovina, S.M.; Hughes, S.G.; Graham, M.J.; Crooke, R.M.; Crooke, S.T.; Witztum, J.L.; Stroes, E.S.; Tsimikas, S. Antisense oligonucleotides targeting apolipoprotein(a) in people with raised lipoprotein(a): two randomised, double-blind, placebo-controlled, dose-ranging trials. Lancet, 2016, 388(10057), 2239-2253.
[126]
Campbell, L.A.; Rosenfeld, M.E. Infection and atherosclerosis development. Arch. Med. Res., 2015, 46(5), 339-350.
[127]
Stary, H.C.; Chandler, A.B.; Glagov, S.; Guyton, J.R.; Insull, W., Jr; Rosenfeld, M.E.; Schaffer, S.A.; Schwartz, C.J.; Wagner, W.D.; Wissler, R.W. A definition of initial, fatty streak, and intermediate lesions of atherosclerosis. A report from the Committee on Vascular Lesions of the Council on Arteriosclerosis, American Heart Association. Circulation, 1994, 89(5), 2462-2478.
[128]
Jonasson, L.; Holm, J.; Skalli, O.; Bondjers, G.; Hansson, G.K. Regional accumulations of T cells, macrophages, and smooth muscle cells in the human atherosclerotic plaque. Arteriosclerosis, 1986, 6(2), 131-138.
[129]
Kovanen, P.T.; Kaartinen, M.; Paavonen, T. Infiltrates of activated mast cells at the site of coronary atheromatous erosion or rupture in myocardial infarction. Circulation, 1995, 92(5), 1084-1088.
[130]
Gutstein, D.E.; Fuster, V. Pathophysiology and clinical significance of atherosclerotic plaque rupture. Cardiovasc. Res., 1999, 41(2), 323-333.
[131]
Ridker, P.M.; Rifai, N.; Rose, L.; Buring, J.E.; Cook, N.R. Comparison of C-reactive protein and low-density lipoprotein cholesterol levels in the prediction of first cardiovascular events. N. Engl. J. Med., 2002, 347(20), 1557-1565.
[132]
Stylianou, I.M.; Bauer, R.C.; Reilly, M.P.; Rader, D.J. Genetic basis of atherosclerosis: insights from mice and humans. Circ. Res., 2012, 110(2), 337-355.
[133]
Roberts, C.K.; Ng, C.; Hama, S.; Eliseo, A.J.; Barnard, R.J. Effect of a short-term diet and exercise intervention on inflammatory/anti-inflammatory properties of HDL in overweight/obese men with cardiovascular risk factors. J. Appl. Physiol., 2006, 101(6), 1727-1732.
[134]
Navab, M.; Anantharamaiah, G.M.; Reddy, S.T.; Hama, S.; Hough, G.; Grijalva, V.R.; Wagner, A.C.; Frank, J.S.; Datta, G.; Garber, D.; Fogelman, A.M. Oral D-4F causes formation of pre-beta high-density lipoprotein and improves high-density lipoprotein-mediated cholesterol efflux and reverse cholesterol transport from macrophages in apolipoprotein E-null mice. Circulation, 2004, 109(25), 3215-3220.
[135]
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.
[136]
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.
[137]
Nofer, J.R.; Assmann, G. Atheroprotective effects of high-density lipoprotein-associated lysosphingolipids. Trends Cardiovasc. Med., 2005, 15(7), 265-271.
[138]
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-kappa B activation in smooth muscle cells. FASEB J., 2003, 17(6), 743-745.
[139]
Xia, P.; Vadas, M.A.; Rye, K.A.; Barter, P.J.; Gamble, J.R. High density lipoproteins (HDL) interrupt the sphingosine kinase signaling pathway. A possible mechanism for protection against atherosclerosis by HDL. J. Biol. Chem., 1999, 274(46), 33143-33147.
[140]
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.
[141]
Sugatani, J.; Miwa, M.; Komiyama, Y.; Ito, S. High-density lipoprotein inhibits the synthesis of platelet-activating factor in human vascular endothelial cells. J. Lipid Mediat. Cell Signal., 1996, 13(1), 73-88.
[142]
Wadham, C.; Albanese, N.; Roberts, J.; Wang, L.; Bagley, C.J.; Gamble, J.R.; Rye, K.A.; Barter, P.J.; Vadas, M.A.; Xia, P. High-density lipoproteins neutralize C-reactive protein proinflammatory activity. Circulation, 2004, 109(17), 2116-2122.
[143]
Furnkranz, A.; Schober, A.; Bochkov, V.N.; Bashtrykov, P.; Kronke, G.; Kadl, A.; Binder, B.R.; Weber, C.; Leitinger, N. Oxidized phospholipids trigger atherogenic inflammation in murine arteries. Arterioscler. Thromb. Vasc. Biol., 2005, 25(3), 633-638.
[144]
Stary, H.C. Natural history and histological classification of atherosclerotic lesions: an update. Arterioscler. Thromb. Vasc. Biol., 2000, 20(5), 1177-1178.
[145]
Virmani, R.; Kolodgie, F.D.; Burke, A.P.; Farb, A.; Schwartz, S.M. Lessons from sudden coronary death: a comprehensive morphological classification scheme for atherosclerotic lesions. Arterioscler. Thromb. Vasc. Biol., 2000, 20(5), 1262-1275.
[146]
Hansson, G.K.; Hermansson, A. The immune system in atherosclerosis. Nat. Immunol., 2011, 12(3), 204-212.
[147]
Simionescu, M. Implications of early structural-functional changes in the endothelium for vascular disease. Arterioscler. Thromb. Vasc. Biol., 2007, 27(2), 266-274.
[148]
Simionescu, M.; Popov, D.; Sima, A. Endothelial transcytosis in health and disease. Cell Tissue Res., 2009, 335(1), 27-40.
[149]
Simionescu, M.; Simionescu, N.; Silbert, J.E.; Palade, G.E. Differentiated microdomains on the luminal surface of the capillary endothelium. II. Partial characterization of their anionic sites. J. Cell Biol., 1981, 90(3), 614-621.
[150]
Gimbrone, M.A., Jr; García-Cardeña, G. Endothelial cell dysfunction and the pathobiology of atherosclerosis. Circ. Res., 2016, 118(4), 620-636.
[151]
Simionescu, N.; Vasile, E.; Lupu, F.; Popescu, G.; Simionescu, M. Prelesional events in atherogenesis. Accumulation of extracellular cholesterol-rich liposomes in the arterial intima and cardiac valves of the hyperlipidemic rabbit. Am. J. Pathol., 1986, 123(1), 109-125.
[152]
Simionescu, N.; Mora, R.; Vasile, E.; Lupu, F.; Filip, D.A.; Simionescu, M. Prelesional modifications of the vessel wall in hyperlipidemic atherogenesis. Extracellular accumulation of modified and reassembled lipoproteins. Ann. N. Y. Acad. Sci., 1990, 598, 1-16.
[153]
Kakutani, M.; Masaki, T.; Sawamura, T. A platelet-endothelium interaction mediated by lectin-like oxidized low-density lipoprotein receptor-1. Proc. Natl. Acad. Sci. USA, 2000, 97(1), 360-364.
[154]
Mukherjee, S.; Coaxum, S.D.; Maleque, M.; Das, S.K. Effects of oxidized low density lipoprotein on nitric oxide synthetase and protein kinase C activities in bovine endothelial cells. Cell. Mol. Biol., 2001, 47(6), 1051-1058.
[155]
Rosenfeld, M.E.; Campbell, L.A. Pathogens and atherosclerosis: update on the potential contribution of multiple infectious organisms to the pathogenesis of atherosclerosis. Thromb. Haemost., 2011, 106(5), 858-867.
[156]
Kuo, C.C.; Shor, A.; Campbell, L.A.; Fukushi, H.; Patton, D.L.; Grayston, J.T. Demonstration of Chlamydia pneumoniae in atherosclerotic lesions of coronary arteries. J. Infect. Dis., 1993, 167(4), 841-849.
[157]
Campbell, L.A.; O’Brien, E.R.; Cappuccio, A.L.; Kuo, C.C.; Wang, S.P.; Stewart, D.; Patton, D.L.; Cummings, P.K.; Grayston, J.T. Detection of Chlamydia pneumoniae TWAR in human coronary atherectomy tissues. J. Infect. Dis., 1995, 172(2), 585-588.
[158]
Shor, A.; Kuo, C.C.; Patton, D.L. Detection of Chlamydia pneumoniae in coronary arterial fatty streaks and atheromatous plaques. S. Afr. Med. J., 1992, 82(3), 158-161.
[159]
Chiu, B. Multiple infections in carotid atherosclerotic plaques. Am. Heart J., 1999, 138(5 Pt 2), S534-S536.
[160]
Ford, P.J.; Gemmell, E.; Chan, A.; Carter, C.L.; Walker, P.J.; Bird, P.S.; West, M.J.; Cullinan, M.P.; Seymour, G.J. Inflammation, heat shock proteins and periodontal pathogens in atherosclerosis: an immunohistologic study. Oral Microbiol. Immunol., 2006, 21(4), 206-211.
[161]
Haraszthy, V.I.; Zambon, J.J.; Trevisan, M.; Zeid, M.; Genco, R.J. Identification of periodontal pathogens in atheromatous plaques. J. Periodontol., 2000, 71(10), 1554-1560.
[162]
Reszka, E.; Jegier, B.; Wasowicz, W.; Lelonek, M.; Banach, M.; Jaszewski, R. Detection of infectious agents by polymerase chain reaction in human aortic wall. Cardiovasc. Pathol., 2008, 17(5), 297-302.
[163]
Latsios, G.; Saetta, A.; Michalopoulos, N.V.; Agapitos, E.; Patsouris, E. Detection of cytomegalovirus, Helicobacter pylori and Chlamydia pneumoniae DNA in carotid atherosclerotic plaques by the polymerase chain reaction. Acta Cardiol., 2004, 59(6), 652-657.
[164]
Pucar, A.; Milasin, J.; Lekovic, V.; Vukadinovic, M.; Ristic, M.; Putnik, S.; Kenney, E.B. Correlation between atherosclerosis and periodontal putative pathogenic bacterial infections in coronary and internal mammary arteries. J. Periodontol., 2007, 78(4), 677-682.
[165]
Rose, J.R.; Mullarkey, M.A.; Christ, W.J.; Hawkins, L.D.; Lynn, M.; Kishi, Y.; Wasan, K.M.; Peteherych, K.; Rossignol, D.P. Consequences of interaction of a lipophilic endotoxin antagonist with plasma lipoproteins. Antimicrob. Agents Chemother., 2000, 44(3), 504-510.
[166]
Murch, O.; Collin, M.; Hinds, C.J.; Thiemermann, C. Lipoproteins in inflammation and sepsis. I. Basic science. Intensive Care Med., 2007, 33(1), 13-24.
[167]
Poelvoorde, P.; Vanhamme, L.; Van Den Abbeele, J.; Switzer, W.M.; Pays, E. Distribution of apolipoprotein L-I and trypanosome lytic activity among primate sera. Mol. Biochem. Parasitol., 2004, 134(1), 155-157.
[168]
Gabay, C.; Kushner, I. Acute-phase proteins and other systemic responses to inflammation. N. Engl. J. Med., 1999, 340(6), 448-454.
[169]
Thaveeratitham, P.; Khovidhunkit, W.; Patumraj, S. High-density lipoproteins (HDL) inhibit endotoxin-induced leukocyte adhesion on endothelial cells in rats: effect of the acute-phase HDL. Clin. Hemorheol. Microcirc., 2007, 36(1), 1-12.
[170]
Berbée, J.F.; van der Hoogt, C.C.; Kleemann, R.; Schippers, E.F.; Kitchens, R.L.; van Dissel, J.T.; Bakker-Woudenberg, I.A.; Havekes, L.M.; Rensen, P.C. Apolipoprotein CI stimulates the response to lipopolysaccharide and reduces mortality in gram-negative sepsis. FASEB J., 2006, 20(12), 2162-2164.
[171]
Nicholls, S.J.; Lundman, P.; Harmer, J.A.; Cutri, B.; Griffiths, K.A.; Rye, K.A.; Barter, P.J.; Celermajer, D.S. Consumption of saturated fat impairs the anti-inflammatory properties of high-density lipoproteins and endothelial function. J. Am. Coll. Cardiol., 2006, 48(4), 715-720.
[172]
Tall, A.R.; Yvan-Charvet, L.; Wang, N. The failure of torcetrapib: was it the molecule or the mechanism? Arterioscler. Thromb. Vasc. Biol., 2007, 27(2), 257-260.
[173]
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.
[174]
Navab, M.; Ananthramaiah, G.M.; Reddy, S.T.; Van Lenten, B.J.; Ansell, B.J.; Hama, S.; Hough, G.; Bachini, E.; Grijalva, V.R.; Wagner, A.C.; Shaposhnik, Z.; Fogelman, A.M. The double jeopardy of HDL. Ann. Med., 2005, 37(3), 173-178.
[175]
Huang, Y.; DiDonato, J.A.; Levison, B. S.; Schmitt, D.; Li, L.; Wu, Y.; Buffa, J.; Kim, T.; Gerstenecker, G. S.; Gu, X.; Kadiyala, C. S.; Wang, Z.; Culley, M. K.; Hazen, J. E.; Didonato, A. J.; Fu, X.; Berisha, S. Z.; Peng, D.; Nguyen,donato, A. J.; Fu, X.; Berisha, S. Z.; Peng, D.; Nguyen, T. T.; Liang, S.; Chuang, C. C.; Cho, L.; Plow, E. F.; Fox, P. L.; Gogonea, V.; Tang, W. H.; Parks, J. S.; Fisher, E. A.; Smith, J. D.; Hazen, S. L An abundant dysfunctional apolipoprotein A1 in human atheroma. Nat. Med., 2014, 20(2), 193-203.
[176]
Roberts, C.K.; Ng, C.; Hama, S.; Eliseo, A.J.; Barnard, R.J. Effect of a short-term diet and exercise intervention on inflammatory/anti-inflammatory properties of HDL in overweight/obese men with cardiovascular risk factors. J. Appl. Physiol., 2006, 101(6), 1727-1732.
[177]
Sirtori, C.R.; Calabresi, L.; Franceschini, G.; Baldassarre, D.; Amato, M.; Johansson, J.; Salvetti, M.; Monteduro, C.; Zulli, R.; Muiesan, M.L.; Agabiti-Rosei, E. Cardiovascular status of carriers of the apolipoprotein A-I(Milano) mutant: the Limone sul Garda study. Circulation, 2001, 103(15), 1949-1954.
[178]
Wolfrum, C.; Poy, M.N.; Stoffel, M. Apolipoprotein M is required for prebeta-HDL formation and cholesterol efflux to HDL and protects against atherosclerosis. Nat. Med., 2005, 11(4), 418-422.
[179]
Christoffersen, C.; Nielsen, L.B.; Axler, O.; Andersson, A.; Johnsen, A.H.; Dahlbäck, B. Isolation and characterization of human apolipoprotein M-containing lipoproteins. J. Lipid Res., 2006, 47(8), 1833-1843.
[180]
Imaizumi, S.; Navab, M.; Morgantini, C.; Charles-Schoeman, C.; Su, F.; Gao, F.; Kwon, M.; Ganapathy, E.; Meriwether, D.; Farias-Eisner, R.; Fogelman, A.M.; Reddy, S.T. Dysfunctional high-density lipoprotein and the potential of apolipoprotein A-1 mimetic peptides to normalize the composition and function of lipoproteins. Circ. J., 2011, 75(7), 1533-1538.

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