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Current Cardiology Reviews

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ISSN (Print): 1573-403X
ISSN (Online): 1875-6557

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Review Article

Regulation of Myocardial Extracellular Matrix Dynamic Changes in Myocardial Infarction and Postinfarct Remodeling

Author(s): Alexey Ushakov, Vera Ivanchenko* and Alina Gagarina

Volume 16, Issue 1, 2020

Page: [11 - 24] Pages: 14

DOI: 10.2174/1573403X15666190509090832

Price: $65

Abstract

The article represents literature review dedicated to molecular and cellular mechanisms underlying clinical manifestations and outcomes of acute myocardial infarction. Extracellular matrix adaptive changes are described in detail as one of the most important factors contributing to healing of damaged myocardium and post-infarction cardiac remodeling. Extracellular matrix is reviewed as dynamic constantly remodeling structure that plays a pivotal role in myocardial repair. The role of matrix metalloproteinases and their tissue inhibitors in fragmentation and degradation of extracellular matrix as well as in myocardium healing is discussed. This review provides current information about fibroblasts activity, the role of growth factors, particularly transforming growth factor β and cardiotrophin-1, colony-stimulating factors, adipokines and gastrointestinal hormones, various matricellular proteins. In conclusion considering the fact that dynamic transformation of extracellular matrix after myocardial ischemic damage plays a pivotal role in myocardial infarction outcomes and prognosis, we suggest a high importance of further investigation of mechanisms underlying extracellular matrix remodeling and cell-matrix interactions in cardiovascular diseases.

Keywords: Myocardial infarction, cardiac remodeling, ECM, cytokines, matricellular proteins, cellular mechanisms.

Graphical Abstract

[1]
Mozaffarian D, Benjamin EJ, Go AS, et al. Heart disease and stroke statistics--2015 update: A report from the American Heart Association. Circulation 2015; 131(4): e29-e322.
[http://dx.doi.org/10.1161/CIR.0000000000000152] [PMID: 25520374]
[2]
Nascimento BR, Brant LC, Moraes DN, Ribeiro AL. Global health and cardiovascular disease. Heart 2014; 100(22): 1743-9.
[http://dx.doi.org/10.1136/heartjnl-2014-306026] [PMID: 25327515]
[3]
Dobaczewski M, Gonzalez-Quesada C, Frangogiannis NG. The extracellular matrix as a modulator of the inflammatory and reparative response following myocardial infarction. J Mol Cell Cardiol 2010; 48(3): 504-11.
[http://dx.doi.org/10.1016/j.yjmcc.2009.07.015] [PMID: 19631653]
[4]
Bahit MC, Kochar A, Granger CB. Post-Myocardial Infarction Heart Failure. JACC Heart Fail 2018; 6(3): 179-86.
[http://dx.doi.org/10.1016/j.jchf.2017.09.015] [PMID: 29496021]
[5]
Miyoshi H, Oishi Y, Mizuguchi Y, et al. Association of left atrial reservoir function with left atrial structural remodeling related to left ventricular dysfunction in asymptomatic patients with hypertension: evaluation by two-dimensional speckle-tracking echocardiography. Clin Exp Hypertens 2015; 37(2): 155-65.
[http://dx.doi.org/10.3109/10641963.2014.933962] [PMID: 25050647]
[6]
Deschamps AM, Spinale FG. Matrix modulation and heart failure: new concepts question old beliefs. Curr Opin Cardiol 2005; 20(3): 211-6.
[http://dx.doi.org/10.1097/01.hco.0000162397.44843.83] [PMID: 15861009]
[7]
Jugdutt BI. Ventricular remodeling after infarction and the extracellular collagen matrix: When is enough enough? Circulation 2003; 108(11): 1395-403.
[http://dx.doi.org/10.1161/01.CIR.0000085658.98621.49] [PMID: 12975244]
[8]
Frangogiannis NG. Pathophysiology of myocardial infarction. Compr Physiol 2015; 5(4): 1841-75.
[http://dx.doi.org/10.1002/cphy.c150006] [PMID: 26426469]
[9]
Matsui Y, Morimoto J, Uede T. Role of matricellular proteins in cardiac tissue remodeling after myocardial infarction. World J Biol Chem 2010; 1(5): 69-80.
[http://dx.doi.org/10.4331/wjbc.v1.i5.69] [PMID: 21540992]
[10]
Prabhu SD, Frangogiannis NG. The biological basis for cardiac repair after myocardial infarction: From inflammation to fibrosis. Circ Res 2016; 119(1): 91-112.
[http://dx.doi.org/10.1161/CIRCRESAHA.116.303577] [PMID: 27340270]
[11]
Lindsey ML, Zamilpa R. Temporal and spatial expression of matrix metalloproteinases and tissue inhibitors of metalloproteinases following myocardial infarction. Cardiovasc Ther 2012; 30(1): 31-41.
[http://dx.doi.org/10.1111/j.1755-5922.2010.00207.x] [PMID: 20645986]
[12]
Kandalam V, Basu R, Abraham T, et al. Early activation of matrix metalloproteinases underlies the exacerbated systolic and diastolic dysfunction in mice lacking TIMP3 following myocardial infarction. Am J Physiol Heart Circ Physiol 2010; 299(4): H1012-23.
[http://dx.doi.org/10.1152/ajpheart.00246.2010] [PMID: 20675565]
[13]
Kandalam V, Basu R, Abraham T, et al. TIMP2 deficiency accelerates adverse post-myocardial infarction remodeling because of enhanced MT1-MMP activity despite lack of MMP2 activation. Circ Res 2010; 106(4): 796-808.
[http://dx.doi.org/10.1161/CIRCRESAHA.109.209189] [PMID: 20056917]
[14]
Koenig GC, Rowe RG, Day SM, et al. MT1-MMP-dependent remodeling of cardiac extracellular matrix structure and function following myocardial infarction. Am J Pathol 2012; 180(5): 1863-78.
[http://dx.doi.org/10.1016/j.ajpath.2012.01.022] [PMID: 22464947]
[15]
Cleutjens JPM, Kandala JC, Guarda E, Guntaka RV, Weber KT. Regulation of collagen degradation in the rat myocardium after infarction. J Mol Cell Cardiol 1995; 27(6): 1281-92.
[http://dx.doi.org/10.1016/S0022-2828(05)82390-9] [PMID: 8531210]
[16]
Heymans S, Luttun A, Nuyens D, et al. Inhibition of plasminogen activators or matrix metalloproteinases prevents cardiac rupture but impairs therapeutic angiogenesis and causes cardiac failure. Nat Med 1999; 5(10): 1135-42.
[http://dx.doi.org/10.1038/13459] [PMID: 10502816]
[17]
Chiao YA, Ramirez TA, Zamilpa R, et al. Matrix metalloproteinase-9 deletion attenuates myocardial fibrosis and diastolic dysfunction in ageing mice. Cardiovasc Res 2012; 96(3): 444-55.
[http://dx.doi.org/10.1093/cvr/cvs275] [PMID: 22918978]
[18]
Zamilpa R, Ibarra J, de Castro Brás LE, et al. Transgenic overexpression of matrix metalloproteinase-9 in macrophages attenuates the inflammatory response and improves left ventricular function post-myocardial infarction. J Mol Cell Cardiol 2012; 53(5): 599-608.
[http://dx.doi.org/10.1016/j.yjmcc.2012.07.017] [PMID: 22884843]
[19]
Ma Y, Chiao YA, Clark R, et al. Deriving a cardiac ageing signature to reveal MMP-9-dependent inflammatory signalling in senescence. Cardiovasc Res 2015; 106(3): 421-31.
[http://dx.doi.org/10.1093/cvr/cvv128] [PMID: 25883218]
[20]
Frieler RA, Mortensen RM. Immune cell and other noncardiomyocyte regulation of cardiac hypertrophy and remodeling. Circulation 2015; 131(11): 1019-30.
[http://dx.doi.org/10.1161/CIRCULATIONAHA.114.008788] [PMID: 25779542]
[21]
Yu Q, Watson RR, Marchalonis JJ, Larson DF. A role for T lymphocytes in mediating cardiac diastolic function. Am J Physiol Heart Circ Physiol 2005; 289(2): H643-51.
[http://dx.doi.org/10.1152/ajpheart.00073.2005] [PMID: 16014617]
[22]
Hinz B, Phan SH, Thannickal VJ, et al. Recent developments in myofibroblast biology: Paradigms for connective tissue remodeling. Am J Pathol 2012; 180(4): 1340-55.
[http://dx.doi.org/10.1016/j.ajpath.2012.02.004] [PMID: 22387320]
[23]
Krenning G, Zeisberg EM, Kalluri R. The origin of fibroblasts and mechanism of cardiac fibrosis. J Cell Physiol 2010; 225(3): 631-7.
[http://dx.doi.org/10.1002/jcp.22322] [PMID: 20635395]
[24]
Turner NA, Porter KE. Function and fate of myofibroblasts after myocardial infarction. Fibrogen Tissue Rep 2013; 6(1): 5.
[http://dx.doi.org/10.1186/1755-1536-6-5] [PMID: 23448358]
[25]
Fan D, Takawale A, Lee J, Kassiri Z. Cardiac fibroblasts, fibrosis and extracellular matrix remodeling in heart disease. Fibrogenesis Tissue Repair 2012; 5(1): 15-28.
[http://dx.doi.org/10.1186/1755-1536-5-15] [PMID: 22943504]
[26]
Ma Y, Halade GV, Lindsey ML. Extracellular matrix and fibroblast communication following myocardial infarction. J Cardiovasc Transl Res 2012; 5(6): 848-57.
[http://dx.doi.org/10.1007/s12265-012-9398-z] [PMID: 22926488]
[27]
Zavadzkas JA, Mukherjee R, Rivers WT, et al. Direct regulation of membrane type 1 matrix metalloproteinase following myocardial infarction causes changes in survival, cardiac function, and remodeling. Am J Physiol Heart Circ Physiol 2011; 301(4): H1656-66.
[http://dx.doi.org/10.1152/ajpheart.00141.2011] [PMID: 21666120]
[28]
Wang ZF, Wang NP, Harmouche S, et al. Postconditioning promotes the cardiac repair through balancing collagen degradation and synthesis after myocardial infarction in rats. Basic Res Cardiol 2013; 108(1): 318-27.
[http://dx.doi.org/10.1007/s00395-012-0318-9] [PMID: 23203208]
[29]
Okada M, Oba Y, Yamawaki H. Endostatin stimulates proliferation and migration of adult rat cardiac fibroblasts through PI3K/Akt pathway. Eur J Pharmacol 2015; 750: 20-6.
[http://dx.doi.org/10.1016/j.ejphar.2015.01.019] [PMID: 25620135]
[30]
Dobaczewski M, de Haan JJ, Frangogiannis NG. The extracellular matrix modulates fibroblast phenotype and function in the infarcted myocardium. J Cardiovasc Transl Res 2012; 5(6): 837-47.
[http://dx.doi.org/10.1007/s12265-012-9406-3] [PMID: 22956156]
[31]
Konstandin MH, Völkers M, Collins B, et al. Fibronectin contributes to pathological cardiac hypertrophy but not physiological growth. Basic Res Cardiol 2013; 108(5)
[http://dx.doi.org/10.1007/s00395-013-0375-8]
[32]
van den Borne SW, Diez J, Blankesteijn WM, Verjans J, Hofstra L, Narula J. Myocardial remodeling after infarction: The role of myofibroblasts. Nat Rev Cardiol 2010; 7(1): 30-7.
[http://dx.doi.org/10.1038/nrcardio.2009.199] [PMID: 19949426]
[33]
Squires CE, Escobar GP, Payne JF, et al. Altered fibroblast function following myocardial infarction. J Mol Cell Cardiol 2005; 39(4): 699-707.
[http://dx.doi.org/10.1016/j.yjmcc.2005.07.008] [PMID: 16111700]
[34]
Frangogiannis NG. The extracellular matrix in myocardial injury, repair, and remodeling. J Clin Invest 2017; 127(5): 1600-12.
[http://dx.doi.org/10.1172/JCI87491] [PMID: 28459429]
[35]
Jousset F, Maguy A, Rohr S, Kucera JP. Myofibroblasts electrotonically coupled to cardiomyocytes alter conduction: Insights at the cellular level from a detailed in silico tissue structure model. Front Physiol 2016; 7: 496.
[http://dx.doi.org/10.3389/fphys.2016.00496] [PMID: 27833567]
[36]
Lighthouse JK, Small EM. Transcriptional control of cardiac fibroblast plasticity. J Mol Cell Cardiol 2016; 91: 52-60.
[http://dx.doi.org/10.1016/j.yjmcc.2015.12.016] [PMID: 26721596]
[37]
Tian J, An X, Niu L. Myocardial fibrosis in congenital and pediatric heart disease. Exp Ther Med 2017; 13(5): 1660-4.
[http://dx.doi.org/10.3892/etm.2017.4224] [PMID: 28565750]
[38]
Frangogiannis NG, Michael LH, Entman ML. Myofibroblasts in reperfused myocardial infarcts express the embryonic form of smooth muscle myosin heavy chain (SMemb). Cardiovasc Res 2000; 48(1): 89-100.
[http://dx.doi.org/10.1016/S0008-6363(00)00158-9] [PMID: 11033111]
[39]
Frangogiannis NG, Shimoni S, Chang SM, et al. Active interstitial remodeling: an important process in the hibernating human myocardium. J Am Coll Cardiol 2002; 39(9): 1468-74.
[http://dx.doi.org/10.1016/S0735-1097(02)01792-8] [PMID: 11985909]
[40]
Willems IE, Havenith MG, De Mey JG, Daemen MJ. The alpha-smooth muscle actin-positive cells in healing human myocardial scars. Am J Pathol 1994; 145(4): 868-75.
[PMID: 7943177]
[41]
Huebener P, Abou-Khamis T, Zymek P, et al. CD44 is critically involved in infarct healing by regulating the inflammatory and fibrotic response. J Immunol 2008; 180(4): 2625-33.
[http://dx.doi.org/10.4049/jimmunol.180.4.2625] [PMID: 18250474]
[42]
Serini G, Gabbiani G. Mechanisms of myofibroblast activity and phenotypic modulation. Exp Cell Res 1999; 250(2): 273-83.
[http://dx.doi.org/10.1006/excr.1999.4543] [PMID: 10413583]
[43]
Nah DY, Rhee MY. The inflammatory response and cardiac repair after myocardial infarction. Korean Circ J 2009; 39(10): 393-8.
[http://dx.doi.org/10.4070/kcj.2009.39.10.393] [PMID: 19949583]
[44]
Bujak M, Dobaczewski M, Chatila K, et al. Interleukin-1 receptor type I signaling critically regulates infarct healing and cardiac remodeling. Am J Pathol 2008; 173(1): 57-67.
[http://dx.doi.org/10.2353/ajpath.2008.070974] [PMID: 18535174]
[45]
Wang F, Trial J, Diwan A, et al. Regulation of cardiac fibroblast cellular function by leukemia inhibitory factor. J Mol Cell Cardiol 2002; 34(10): 1309-16.
[http://dx.doi.org/10.1006/jmcc.2002.2059] [PMID: 12392991]
[46]
Pepper MS, Ferrara N, Orci L, Montesano R. Leukemia inhibitory factor (LIF) inhibits angiogenesis in vitro. J Cell Sci 1995; 108(Pt 1): 73-83.
[PMID: 7537748]
[47]
Sun Y, Weber KT. Infarct scar: a dynamic tissue. Cardiovasc Res 2000; 46(2): 250-6.
[http://dx.doi.org/10.1016/S0008-6363(00)00032-8] [PMID: 10773228]
[48]
Zhang J, Fan G, Zhao H, et al. Targeted inhibition of focal adhesion kinase attenuates cardiac fibrosis and preserves heart function in adverse cardiac remodeling. Sci Rep 2017; 7: 43146.
[http://dx.doi.org/10.1038/srep43146] [PMID: 28225063]
[49]
Moore JB IV, Zhao J, Fischer AG, et al. Histone deacetylase 1 depletion activates human cardiac mesenchymal stromal cell proangiogenic paracrine signaling through a mechanism requiring enhanced basic fibroblast growth factor synthesis and secretion. J Am Heart Assoc 2017; 6(7)e006183
[http://dx.doi.org/10.1161/JAHA.117.006183] [PMID: 28679560]
[50]
Ushikoshi H, Takahashi T, Chen X, et al. Local overexpression of HB-EGF exacerbates remodeling following myocardial infarction by activating noncardiomyocytes. Lab Invest 2005; 85(7): 862-73.
[http://dx.doi.org/10.1038/labinvest.3700282] [PMID: 15856048]
[51]
Koshman YE, Sternlicht MD, Kim T, et al. Connective tissue growth factor regulates cardiac function and tissue remodeling in a mouse model of dilated cardiomyopathy. J Mol Cell Cardiol 2015; 89(Pt B): 214-22.
[http://dx.doi.org/10.1016/j.yjmcc.2015.11.003] [PMID: 26549358]
[52]
Liu XH, Pan LL, Deng HY, et al. Leonurine (SCM-198) attenuates myocardial fibrotic response via inhibition of NADPH oxidase 4. Free Radic Biol Med 2013; 54: 93-104.
[http://dx.doi.org/10.1016/j.freeradbiomed.2012.10.555] [PMID: 23127783]
[53]
Shinde AV, Frangogiannis NG. Fibroblasts in myocardial infarction: a role in inflammation and repair. J Mol Cell Cardiol 2014; 70: 74-82.
[http://dx.doi.org/10.1016/j.yjmcc.2013.11.015] [PMID: 24321195]
[54]
Frangogiannis NG. The role of transforming growth factor (TGF)-β in the infarcted myocardium. J Thorac Dis 2017; 9(1): S52-63.
[http://dx.doi.org/10.21037/jtd.2016.11.19] [PMID: 28446968]
[55]
Frangogiannis NG. Matricellular proteins in cardiac adaptation and disease. Physiol Rev 2012; 92(2): 635-88.
[http://dx.doi.org/10.1152/physrev.00008.2011] [PMID: 22535894]
[56]
Dobaczewski M, Chen W, Frangogiannis NG. Transforming growth factor (TGF)-β signaling in cardiac remodeling. J Mol Cell Cardiol 2011; 51(4): 600-6.
[http://dx.doi.org/10.1016/j.yjmcc.2010.10.033] [PMID: 21059352]
[57]
Sarrazy V, Koehler A, Chow ML, et al. Integrins αvβ5 and αvβ3 promote latent TGF-β1 activation by human cardiac fibroblast contraction. Cardiovasc Res 2014; 102(3): 407-17.
[http://dx.doi.org/10.1093/cvr/cvu053] [PMID: 24639195]
[58]
Frantz S, Hu K, Adamek A, et al. Transforming growth factor beta inhibition increases mortality and left ventricular dilatation after myocardial infarction. Basic Res Cardiol 2008; 103(5): 485-92.
[http://dx.doi.org/10.1007/s00395-008-0739-7] [PMID: 18651091]
[59]
Svystonyuk DA, Ngu JM, Mewhort HE, et al. Fibroblast growth factor-2 regulates human cardiac myofibroblast-mediated extracellular matrix remodeling. J Transl Med 2015; 13: 147.
[http://dx.doi.org/10.1186/s12967-015-0510-4] [PMID: 25948488]
[60]
Virag JA, Rolle ML, Reece J, Hardouin S, Feigl EO, Murry CE. Fibroblast growth factor-2 regulates myocardial infarct repair: Effects on cell proliferation, scar contraction, and ventricular function. Am J Pathol 2007; 171(5): 1431-40.
[http://dx.doi.org/10.2353/ajpath.2007.070003] [PMID: 17872976]
[61]
Zhao T, Zhao W, Chen Y, Li VS, Meng W, Sun Y. Platelet-derived growth factor-D promotes fibrogenesis of cardiac fibroblasts. Am J Physiol Heart Circ Physiol 2013; 304(12): H1719-26.
[http://dx.doi.org/10.1152/ajpheart.00130.2013] [PMID: 23585135]
[62]
Zymek P, Bujak M, Chatila K, et al. The role of platelet-derived growth factor signaling in healing myocardial infarcts. J Am Coll Cardiol 2006; 48(11): 2315-23.
[http://dx.doi.org/10.1016/j.jacc.2006.07.060] [PMID: 17161265]
[63]
Awada HK, Johnson NR, Wang Y. Sequential delivery of angiogenic growth factors improves revascularization and heart function after myocardial infarction. J Control Release 2015; 207: 7-17.
[http://dx.doi.org/10.1016/j.jconrel.2015.03.034] [PMID: 25836592]
[64]
Bry M, Kivelä R, Leppänen VM, Alitalo K. Vascular endothelial growth factor-B in physiology and disease. Physiol Rev 2014; 94(3): 779-94.
[http://dx.doi.org/10.1152/physrev.00028.2013] [PMID: 24987005]
[65]
Hogas S, Bilha SC, Branisteanu D, et al. Potential novel biomarkers of cardiovascular dysfunction and disease: Cardiotrophin-1, adipokines and galectin-3. Arch Med Sci 2017; 13(4): 897-913.
[http://dx.doi.org/10.5114/aoms.2016.58664] [PMID: 28721158]
[66]
Abdul-Ghani M, Suen C, Jiang B, et al. Cardiotrophin 1 stimulates beneficial myogenic and vascular remodeling of the heart. Cell Res 2017; 27(10): 1195-215.
[http://dx.doi.org/10.1038/cr.2017.87] [PMID: 28785017]
[67]
Pennica D, King KL, Shaw KJ, et al. Expression cloning of cardiotrophin 1, a cytokine that induces cardiac myocyte hypertrophy. Proc Natl Acad Sci USA 1995; 92(4): 1142-6.
[http://dx.doi.org/10.1073/pnas.92.4.1142] [PMID: 7862649]
[68]
López B, González A, Querejeta R, Larman M, Rábago G, Díez J. Association of cardiotrophin-1 with myocardial fibrosis in hypertensive patients with heart failure. Hypertension 2014; 63(3): 483-9.
[http://dx.doi.org/10.1161/HYPERTENSIONAHA.113.02654] [PMID: 24366078]
[69]
Schillaci G, Pucci G, Perlini S. From hypertension to hypertrophy to heart failure: the role of cardiotrophin-1. J Hypertens 2013; 31(3): 474-6.
[http://dx.doi.org/10.1097/HJH.0b013e32835ed4bb] [PMID: 23615209]
[70]
Tecimer ME, Yuksel A, Bicer M, et al. The role of cardiotrophin-1 in the evaluation of myocardial ischemia in patients undergoing off-pump and on-pump coronary artery bypass surgery. Scientific Pages Heart 2016; 1(1): 14-20.
[71]
Aoyama T, Takimoto Y, Pennica D, et al. Augmented expression of cardiotrophin-1 and its receptor component, gp130, in both left and right ventricles after myocardial infarction in the rat. J Mol Cell Cardiol 2000; 32(10): 1821-30.
[http://dx.doi.org/10.1006/jmcc.2000.1218] [PMID: 11013126]
[72]
López B, González A, Lasarte JJ, et al. Is plasma cardiotrophin-1 a marker of hypertensive heart disease? J Hypertens 2005; 23(3): 625-32.
[http://dx.doi.org/10.1097/01.hjh.0000160221.09468.d3] [PMID: 15716706]
[73]
Altun I, Pamukcu B, Yildiz CE, et al. Cardiotrophin-1: A new predictor of atrial fibrillation relapses after successful cardioversion. Bosn J Basic Med Sci 2015; 15(3): 68-73.
[http://dx.doi.org/10.17305/bjbms.2015.503] [PMID: 26295297]
[74]
Al-Mazroua HA, Al-Rasheed NM, Korashy HM. Downregulation of the cardiotrophin-1 gene expression by valsartan and spironolactone in hypertrophied heart rats in vivo and rat cardiomyocyte H9c2 cell line in vitro: A novel mechanism of cardioprotection. J Cardiovasc Pharmacol 2013; 61(4): 337-44.
[http://dx.doi.org/10.1097/FJC.0b013e318283a565] [PMID: 23288202]
[75]
González A, López B, Ravassa S, et al. Cardiotrophin-1 in hypertensive heart disease. Endocrine 2012; 42(1): 9-17.
[http://dx.doi.org/10.1007/s12020-012-9649-4] [PMID: 22418690]
[76]
Robador PA, San José G, Rodríguez C, et al. HIF-1-mediated up-regulation of cardiotrophin-1 is involved in the survival response of cardiomyocytes to hypoxia. Cardiovasc Res 2011; 92(2): 247-55.
[http://dx.doi.org/10.1093/cvr/cvr202] [PMID: 21771897]
[77]
Song K, Wang S, Huang B, Luciano A, Srivastava R, Mani A. Plasma cardiotrophin-1 levels are associated with hypertensive heart disease: A meta-analysis. J Clin Hypertens (Greenwich) 2014; 16(9): 686-92.
[http://dx.doi.org/10.1111/jch.12376] [PMID: 25052897]
[78]
Wollert KC, Taga T, Saito M, et al. Cardiotrophin-1 activates a distinct form of cardiac muscle cell hypertrophy. Assembly of sarcomeric units in series VIA gp130/leukemia inhibitory factor receptor-dependent pathways. J Biol Chem 1996; 271(16): 9535-45.
[http://dx.doi.org/10.1074/jbc.271.16.9535] [PMID: 8621626]
[79]
Aguilar-Melero P, Luque A, Machuca MM, et al. Cardiotrophin-1 reduces ischemia/reperfusion injury during liver transplant. J Surg Res 2013; 181(2): e83-91.
[http://dx.doi.org/10.1016/j.jss.2012.07.046] [PMID: 22906559]
[80]
Calabrò P, Limongelli G, Riegler L, et al. Novel insights into the role of cardiotrophin-1 in cardiovascular diseases. J Mol Cell Cardiol 2009; 46(2): 142-8.
[http://dx.doi.org/10.1016/j.yjmcc.2008.11.002] [PMID: 19059413]
[81]
Freed DH, Cunnington RH, Dangerfield AL, Sutton JS, Dixon IM. Emerging evidence for the role of cardiotrophin-1 in cardiac repair in the infarcted heart. Cardiovasc Res 2005; 65(4): 782-92.
[http://dx.doi.org/10.1016/j.cardiores.2004.11.026] [PMID: 15721858]
[82]
Freed DH, Chilton L, Li Y, et al. Role of myosin light chain kinase in cardiotrophin-1-induced cardiac myofibroblast cell migration. Am J Physiol Heart Circ Physiol 2011; 301(2): H514-22.
[http://dx.doi.org/10.1152/ajpheart.01041.2010] [PMID: 21572008]
[83]
Freed DH, Moon MC, Borowiec AM, Jones SC, Zahradka P, Dixon IM. Cardiotrophin-1: expression in experimental myocardial infarction and potential role in post-MI wound healing. Mol Cell Biochem 2003; 254(1-2): 247-56.
[http://dx.doi.org/10.1023/A:1027332504861] [PMID: 14674704]
[84]
D’Amario D, Leone AM, Cannata F, et al. Granulocyte colony-stimulating factor in patients with a large anterior wall acute myocardial infarction to prevent left ventricular remodeling (the RIGENERA trial): 10 years follow-up - Final results. European Heart Journal 38(1)2017
[85]
D’Amario D, Leone AM, Borovac JA, et al. Granulocyte colony-stimulating factor for the treatment of cardiovascular diseases: An update with a critical appraisal. Pharmacol Res 2018; 127: 67-76.
[http://dx.doi.org/10.1016/j.phrs.2017.06.001] [PMID: 28602846]
[86]
Sugano Y, Anzai T, Yoshikawa T, et al. Granulocyte colony-stimulating factor attenuates early ventricular expansion after experimental myocardial infarction. Cardiovasc Res 2005; 65(2): 446-56.
[http://dx.doi.org/10.1016/j.cardiores.2004.10.008] [PMID: 15639484]
[87]
Yano T, Miura T, Whittaker P, et al. Macrophage colony-stimulating factor treatment after myocardial infarction attenuates left ventricular dysfunction by accelerating infarct repair. J Am Coll Cardiol 2006; 47(3): 626-34.
[http://dx.doi.org/10.1016/j.jacc.2005.09.037] [PMID: 16458148]
[88]
Maekawa Y, Anzai T, Yoshikawa T, et al. Effect of granulocyte-macrophage colony-stimulating factor inducer on left ventricular remodeling after acute myocardial infarction. J Am Coll Cardiol 2004; 44(7): 1510-20.
[http://dx.doi.org/10.1016/j.jacc.2004.05.083] [PMID: 15464336]
[89]
Morishita K, Takemura G, Tsujimoto A, et al. Postinfarction cardiac remodeling proceeds normally in granulocyte colony-stimulating factor knockout mice. Am J Pathol 2015; 185(7): 1899-911.
[http://dx.doi.org/10.1016/j.ajpath.2015.03.018] [PMID: 25976246]
[90]
Ishikawa Y, Akasaka Y, Ishii T, et al. Changes in the distribution pattern of gelatin-binding protein of 28 kDa (adiponectin) in myocardial remodelling after ischaemic injury. Histopathology 2003; 42(1): 43-52.
[http://dx.doi.org/10.1046/j.1365-2559.2003.01518.x] [PMID: 12493024]
[91]
Jenke A, Schur R, Röger C, et al. Adiponectin attenuates profibrotic extracellular matrix remodeling following cardiac injury by up-regulating matrix metalloproteinase 9 expression in mice. Physiol Rep 2017; 5(24)e13523
[http://dx.doi.org/10.14814/phy2.13523] [PMID: 29263115]
[92]
Ghantous CM, Azrak Z, Hanache S, Abou-Kheir W, Zeidan A. Differential role of leptin and adiponectin in cardiovascular system. Int J Endocrinol 2015.2015534320
[http://dx.doi.org/10.1155/2015/534320] [PMID: 26064110]
[93]
McGaffin KR, Sun C-K, Rager JJ, et al. Leptin signalling reduces the severity of cardiac dysfunction and remodelling after chronic ischaemic injury. Cardiovasc Res 2008; 77(1): 54-63.
[http://dx.doi.org/10.1093/cvr/cvm023] [PMID: 18006469]
[94]
Zhang BH, Guo CX, Wang HX, et al. Cardioprotective effects of adipokine apelin on myocardial infarction. Heart Vessels 2014; 29(5): 679-89.
[http://dx.doi.org/10.1007/s00380-013-0425-z] [PMID: 24141989]
[95]
Zhang X, Hu W, Feng F, Xu J, Wu F. Apelin-13 protects against myocardial infarction-induced myocardial fibrosis. Mol Med Rep 2016; 13(6): 5262-8.
[http://dx.doi.org/10.3892/mmr.2016.5163] [PMID: 27109054]
[96]
Pradhan G, Samson SL, Sun Y. Ghrelin: Much more than a hunger hormone. Curr Opin Clin Nutr Metab Care 2013; 16(6): 619-24.
[http://dx.doi.org/10.1097/MCO.0b013e328365b9be] [PMID: 24100676]
[97]
Yuan MJ. He-Huang, Hu HY, Li-Quan, Hong-Jiang, Huang CX. Myocardial angiogenesis after chronic ghrelin treatment in a rat myocardial infarction model. Regul Pept 2012; 179(1-3): 39-42.
[http://dx.doi.org/10.1016/j.regpep.2012.08.013] [PMID: 22960289]
[98]
Mao Y, Tokudome T, Otani K, et al. Ghrelin prevents incidence of malignant arrhythmia after acute myocardial infarction through vagal afferent nerves. Endocrinology 2012; 153(7): 3426-34.
[http://dx.doi.org/10.1210/en.2012-1065] [PMID: 22535766]
[99]
Schellings MW, Pinto YM, Heymans S. Matricellular proteins in the heart: possible role during stress and remodeling. Cardiovasc Res 2004; 64(1): 24-31.
[http://dx.doi.org/10.1016/j.cardiores.2004.06.006] [PMID: 15364610]
[100]
Ma Y, de Castro Brás LE, Toba H, et al. Myofibroblasts and the extracellular matrix network in post-myocardial infarction cardiac remodeling. Pflugers Arch 2014; 466(6): 1113-27.
[http://dx.doi.org/10.1007/s00424-014-1463-9] [PMID: 24519465]
[101]
Bornstein P. Matricellular proteins: An overview. J Cell Commun Signal 2009; 3(3-4): 163-5.
[http://dx.doi.org/10.1007/s12079-009-0069-z] [PMID: 19779848]
[102]
Imanaka-Yoshida K, Hiroe M, Nishikawa T, et al. Tenascin-C modulates adhesion of cardiomyocytes to extracellular matrix during tissue remodeling after myocardial infarction. Lab Invest 2001; 81(7): 1015-24.
[http://dx.doi.org/10.1038/labinvest.3780313] [PMID: 11454990]
[103]
Nishioka T, Onishi K, Shimojo N, et al. Tenascin-C may aggravate left ventricular remodeling and function after myocardial infarction in mice. Am J Physiol Heart Circ Physiol 2010; 298(3): H1072-8.
[http://dx.doi.org/10.1152/ajpheart.00255.2009] [PMID: 20081106]
[104]
Imanaka-Yoshida K. Extracellular matrix remodeling in vascular development and disease2016 Jun 25 Etiology and morphogenesis of congenital heart disease: From Gene Function and Cellular Interaction to Morphology 2016 https://europepmc.org/books/NBK500279;jsessionid=A0E7D81C6A80CC5CF3186C92A2F3B60A [Internet]
[105]
Midwood KS, Orend G. The role of tenascin-C in tissue injury and tumorigenesis. J Cell Commun Signal 2009; 3(3-4): 287-310.
[http://dx.doi.org/10.1007/s12079-009-0075-1] [PMID: 19838819]
[106]
Mao JR, Taylor G, Dean WB, et al. Tenascin-X deficiency mimics Ehlers-Danlos syndrome in mice through alteration of collagen deposition. Nat Genet 2002; 30(4): 421-5.
[http://dx.doi.org/10.1038/ng850] [PMID: 11925569]
[107]
Matsumoto K, Takayama N, Ohnishi J, et al. Tumour invasion and metastasis are promoted in mice deficient in tenascin-X. Genes Cells 2001; 6(12): 1101-11.
[http://dx.doi.org/10.1046/j.1365-2443.2001.00482.x] [PMID: 11737270]
[108]
Bradshaw AD. The role of secreted protein acidic and rich in cysteine (SPARC) in cardiac repair and fibrosis: Does expression of SPARC by macrophages influence outcomes? J Mol Cell Cardiol 2016; 93: 156-61.
[http://dx.doi.org/10.1016/j.yjmcc.2015.11.014] [PMID: 26582465]
[109]
Schellings MW, Vanhoutte D, Swinnen M, et al. Absence of SPARC results in increased cardiac rupture and dysfunction after acute myocardial infarction. J Exp Med 2009; 206(1): 113-23.
[http://dx.doi.org/10.1084/jem.20081244] [PMID: 19103879]
[110]
Rienks M, Papageorgiou AP, Frangogiannis NG, Heymans S. Myocardial extracellular matrix: An ever-changing and diverse entity. Circ Res 2014; 114(5): 872-88.
[http://dx.doi.org/10.1161/CIRCRESAHA.114.302533] [PMID: 24577967]
[111]
McCurdy SM, Dai Q, Zhang J, et al. SPARC mediates early extracellular matrix remodeling following myocardial infarction. Am J Physiol Heart Circ Physiol 2011; 301(2): H497-505.
[http://dx.doi.org/10.1152/ajpheart.01070.2010] [PMID: 21602472]
[112]
Yokosaki Y, Tanaka K, Higashikawa F, Yamashita K, Eboshida A. Distinct structural requirements for binding of the integrins alphavbeta6, alphavbeta3, alphavbeta5, alpha5beta1 and alpha9beta1 to osteopontin. Matrix Biol 2005; 24(6): 418-27.
[http://dx.doi.org/10.1016/j.matbio.2005.05.005] [PMID: 16005200]
[113]
Scatena M, Liaw L, Giachelli CM. Osteopontin: A multifunctional molecule regulating chronic inflammation and vascular disease. Arterioscler Thromb Vasc Biol 2007; 27(11): 2302-9.
[http://dx.doi.org/10.1161/ATVBAHA.107.144824] [PMID: 17717292]
[114]
Trueblood NA, Xie Z, Communal C, et al. Exaggerated left ventricular dilation and reduced collagen deposition after myocardial infarction in mice lacking osteopontin. Circ Res 2001; 88(10): 1080-7.
[http://dx.doi.org/10.1161/hh1001.090842] [PMID: 11375279]
[115]
Xie Z, Singh M, Singh K. ERK1/2 and JNKs, but not p38 kinase, are involved in reactive oxygen species-mediated induction of osteopontin gene expression by angiotensin II and interleukin-1beta in adult rat cardiac fibroblasts. J Cell Physiol 2004; 198(3): 399-407.
[http://dx.doi.org/10.1002/jcp.10419] [PMID: 14755545]
[116]
Lindsey ML, Saucerman JJ, DeLeon-Pennell KY. Knowledge gaps to understanding cardiac macrophage polarization following myocardial infarction. Biochim Biophys Acta 2016; 1862(12): 2288-92.
[http://dx.doi.org/10.1016/j.bbadis.2016.05.013] [PMID: 27240543]
[117]
Dahiya S, Givvimani S, Bhatnagar S, Qipshidze N, Tyagi SC, Kumar A. Osteopontin-stimulated expression of matrix metalloproteinase-9 causes cardiomyopathy in the mdx model of Duchenne muscular dystrophy. J Immunol 2011; 187(5): 2723-31.
[http://dx.doi.org/10.4049/jimmunol.1101342] [PMID: 21810612]
[118]
Sponder M, Fritzer-Szekeres M, Marculescu R, Litschauer B, Strametz-Juranek J. Physical inactivity increases endostatin and osteopontin in patients with coronary artery disease. Heart Vessels 2016; 31(10): 1603-8.
[http://dx.doi.org/10.1007/s00380-015-0778-6] [PMID: 26661073]
[119]
Fujita N, Fujita S, Okada Y, et al. Impaired angiogenic response in the corneas of mice lacking osteopontin. Invest Ophthalmol Vis Sci 2010; 51(2): 790-4.
[http://dx.doi.org/10.1167/iovs.09-3420] [PMID: 19741245]
[120]
Biernacka A, Dobaczewski M, Frangogiannis NG. TGF-β signaling in fibrosis. Growth Factors 2011; 29(5): 196-202.
[http://dx.doi.org/10.3109/08977194.2011.595714] [PMID: 21740331]
[121]
Kirk JA, Cingolani OH. Thrombospondins in the transition from myocardial infarction to heart failure. J Mol Cell Cardiol 2016; 90: 102-10.
[http://dx.doi.org/10.1016/j.yjmcc.2015.12.009] [PMID: 26686988]
[122]
Mustonen E, Ruskoaho H, Rysä J. Thrombospondins, potential drug targets for cardiovascular diseases. Basic Clin Pharmacol Toxicol 2013; 112(1): 4-12.
[http://dx.doi.org/10.1111/bcpt.12026] [PMID: 23074998]
[123]
Calabro NE, Kristofik NJ, Kyriakides TR. Thrombospondin-2 and extracellular matrix assembly. Biochim Biophys Acta 2014; 1840(8): 2396-402.
[http://dx.doi.org/10.1016/j.bbagen.2014.01.013] [PMID: 24440155]
[124]
Cleutjens J, Huynen F, Smits J, et al. Thrombospondin-2 deficiency in mice results in cardiac rupture early after myocardial infarction. Circ Res 1999; 100: 156.
[125]
Shimazaki M, Nakamura K, Kii I, et al. Periostin is essential for cardiac healing after acute myocardial infarction. J Exp Med 2008; 205(2): 295-303.
[http://dx.doi.org/10.1084/jem.20071297] [PMID: 18208976]
[126]
Taniyama Y, Katsuragi N, Sanada F, et al. Selective blockade of periostin exon 17 preserves cardiac performance in acute myocardial infarction. Hypertension 2016; 67(2): 356-61.
[http://dx.doi.org/10.1161/HYPERTENSIONAHA.115.06265] [PMID: 26644236]
[127]
Kaur H, Takefuji M, Ngai CY, et al. Targeted ablation of periostin-expressing activated fibroblasts prevents adverse cardiac remodeling in mice. Circ Res 2016; 118(12): 1906-17.
[http://dx.doi.org/10.1161/CIRCRESAHA.116.308643] [PMID: 27140435]
[128]
Oka T, Xu J, Kaiser RA, et al. Genetic manipulation of periostin expression reveals a role in cardiac hypertrophy and ventricular remodeling. Circ Res 2007; 101(3): 313-21.
[http://dx.doi.org/10.1161/CIRCRESAHA.107.149047] [PMID: 17569887]
[129]
Chen CC, Lau LF. Functions and mechanisms of action of CCN matricellular proteins. Int J Biochem Cell Biol 2009; 41(4): 771-83.
[http://dx.doi.org/10.1016/j.biocel.2008.07.025] [PMID: 18775791]
[130]
Dobaczewski M, Bujak M, Li N, et al. Smad3 signaling critically regulates fibroblast phenotype and function in healing myocardial infarction. Circ Res 2010; 107(3): 418-28.
[http://dx.doi.org/10.1161/CIRCRESAHA.109.216101] [PMID: 20522804]
[131]
Lee CH, Shah B, Moioli EK, Mao JJ. CTGF directs fibroblast differentiation from human mesenchymal stem/stromal cells and defines connective tissue healing in a rodent injury model. J Clin Invest 2010; 120(9): 3340-9.
[http://dx.doi.org/10.1172/JCI43230] [PMID: 20679726]
[132]
Twigg SM. Regulation and bioactivity of the CCN family of genes and proteins in obesity and diabetes. J Cell Commun Signal 2018; 12(1): 359-68.
[http://dx.doi.org/10.1007/s12079-018-0458-2] [PMID: 29411334]
[133]
Ahmed MS, Gravning J, Martinov VN, et al. Mechanisms of novel cardioprotective functions of CCN2/CTGF in myocardial ischemia-reperfusion injury. Am J Physiol Heart Circ Physiol 2011; 300(4): H1291-302.
[http://dx.doi.org/10.1152/ajpheart.00604.2010] [PMID: 21186275]
[134]
Weis SM, Zimmerman SD, Shah M, et al. A role for decorin in the remodeling of myocardial infarction. Matrix Biol 2005; 24(4): 313-24.
[http://dx.doi.org/10.1016/j.matbio.2005.05.003] [PMID: 15949932]
[135]
Melchior-Becker A, Dai G, Ding Z, et al. Deficiency of biglycan causes cardiac fibroblasts to differentiate into a myofibroblast phenotype. J Biol Chem 2011; 286(19): 17365-75.
[http://dx.doi.org/10.1074/jbc.M110.192682] [PMID: 21454527]
[136]
Weir RA, Petrie CJ, Murphy CA, et al. Galectin-3 and cardiac function in survivors of acute myocardial infarction. Circ Heart Fail 2013; 6(3): 492-8.
[http://dx.doi.org/10.1161/CIRCHEARTFAILURE.112.000146] [PMID: 23505301]
[137]
Mayr A, Klug G, Mair J, et al. Galectin-3: relation to infarct scar and left ventricular function after myocardial infarction. Int J Cardiol 2013; 163(3): 335-7.
[http://dx.doi.org/10.1016/j.ijcard.2012.06.087] [PMID: 22795719]
[138]
Vanhoutte D, Schellings MW, Götte M, et al. Increased expression of syndecan-1 protects against cardiac dilatation and dysfunction after myocardial infarction. Circulation 2007; 115(4): 475-82.
[http://dx.doi.org/10.1161/CIRCULATIONAHA.106.644609] [PMID: 17242279]
[139]
Xie J, Wang J, Li R, et al. Syndecan-4 over-expression preserves cardiac function in a rat model of myocardial infarction. J Mol Cell Cardiol 2012; 53(2): 250-8.
[http://dx.doi.org/10.1016/j.yjmcc.2012.04.014] [PMID: 22561100]
[140]
Shetelig C, Limalanathan S, Eritsland J, et al. Osteoprotegerin levels in ST-elevation myocardial infarction: Temporal profile and association with myocardial injury and left ventricular function. PLoS One 2017; 12(3)e0173034
[http://dx.doi.org/10.1371/journal.pone.0173034] [PMID: 28253327]
[141]
Crisafulli A, Micari A, Altavilla D, et al. Serum levels of osteoprotegerin and RANKL in patients with ST elevation acute myocardial infarction. Clin Sci (Lond) 2005; 109(4): 389-95.
[http://dx.doi.org/10.1042/CS20050058] [PMID: 15926884]
[142]
Andersen GO, Knudsen EC, Aukrust P, et al. Elevated serum osteoprotegerin levels measured early after acute ST-elevation myocardial infarction predict final infarct size. Heart 2011; 97(6): 460-5.
[http://dx.doi.org/10.1136/hrt.2010.206714] [PMID: 21270073]
[143]
DeLeon-Pennell KY, Tian Y, Zhang B, et al. Cd36 is a matrix metalloproteinase-9 substrate that stimulates neutrophil apoptosis and removal during cardiac remodeling. Circ Cardiovasc Genet 2016; 9(1): 14-25.
[http://dx.doi.org/10.1161/CIRCGENETICS.115.001249] [PMID: 26578544]
[144]
DeLeon-Pennell KY, Meschiari CA, Jung M, Lindsey ML. Matrix metalloproteinases in myocardial infarction and heart failure. Prog Mol Biol Transl Sci 2017; 147: 75-100.
[http://dx.doi.org/10.1016/bs.pmbts.2017.02.001] [PMID: 28413032]
[145]
Lindsey ML, Gannon J, Aikawa M, et al. Selective matrix metalloproteinase inhibition reduces left ventricular remodeling but does not inhibit angiogenesis after myocardial infarction. Circulation 2002; 105(6): 753-8.
[http://dx.doi.org/10.1161/hc0602.103674] [PMID: 11839633]
[146]
Matsumura S, Iwanaga S, Mochizuki S, Okamoto H, Ogawa S, Okada Y. Targeted deletion or pharmacological inhibition of MMP-2 prevents cardiac rupture after myocardial infarction in mice. J Clin Invest 2005; 115(3): 599-609.
[http://dx.doi.org/10.1172/JCI22304] [PMID: 15711638]
[147]
Hudson MP, Armstrong PW, Ruzyllo W, et al. Effects of selective matrix metalloproteinase inhibitor (PG-116800) to prevent ventricular remodeling after myocardial infarction: Results of the PREMIER (Prevention of Myocardial Infarction Early Remodeling) trial. J Am Coll Cardiol 2006; 48(1): 15-20.
[http://dx.doi.org/10.1016/j.jacc.2006.02.055] [PMID: 16814643]
[148]
Iyer RP, de Castro Brás LE, Patterson NL, et al. Early matrix metalloproteinase-9 inhibition post-myocardial infarction worsens cardiac dysfunction by delaying inflammation resolution. J Mol Cell Cardiol 2016; 100: 109-17.
[http://dx.doi.org/10.1016/j.yjmcc.2016.10.005] [PMID: 27746126]
[149]
Iyer RP, Patterson NL, Zouein FA, et al. Early matrix metalloproteinase-12 inhibition worsens post-myocardial infarction cardiac dysfunction by delaying inflammation resolution. Int J Cardiol 2015; 185: 198-208.
[http://dx.doi.org/10.1016/j.ijcard.2015.03.054] [PMID: 25797678]
[150]
Okada H, Takemura G, Kosai K, et al. Postinfarction gene therapy against transforming growth factor-beta signal modulates infarct tissue dynamics and attenuates left ventricular remodeling and heart failure. Circulation 2005; 111(19): 2430-7.
[http://dx.doi.org/10.1161/01.CIR.0000165066.71481.8E] [PMID: 15867170]
[151]
Biernacka A, Cavalera M, Wang J, et al. Smad3 signaling promotes fibrosis while preserving cardiac and aortic geometry in obese diabetic mice. Circ Heart Fail 2015; 8(4): 788-98.
[http://dx.doi.org/10.1161/CIRCHEARTFAILURE.114.001963] [PMID: 25985794]
[152]
Mann DL, McMurray JJ, Packer M, et al. Targeted anticytokine therapy in patients with chronic heart failure: Results of the Randomized Etanercept Worldwide Evaluation (RENEWAL). Circulation 2004; 109(13): 1594-602.
[http://dx.doi.org/10.1161/01.CIR.0000124490.27666.B2] [PMID: 15023878]
[153]
Somasuntharam I, Yehl K, Carroll SL, et al. Knockdown of TNF-α by DNAzyme gold nanoparticles as an anti-inflammatory therapy for myocardial infarction. Biomaterials 2016; 83: 12-22.
[http://dx.doi.org/10.1016/j.biomaterials.2015.12.022] [PMID: 26773660]
[154]
Abbate A, Van Tassell BW, Biondi-Zoccai G, et al. Effects of interleukin-1 blockade with anakinra on adverse cardiac remodeling and heart failure after acute myocardial infarction [from the Virginia Commonwealth University-Anakinra Remodeling Trial (2) (VCU-ART2) pilot study]. Am J Cardiol 2013; 111(10): 1394-400.
[http://dx.doi.org/ 10.1016/j.amjcard.2013.01.287] [PMID: 23453459]
[155]
Kühn B, del Monte F, Hajjar RJ, et al. Periostin induces proliferation of differentiated cardiomyocytes and promotes cardiac repair. Nat Med 2007; 13(8): 962-9.
[http://dx.doi.org/10.1038/nm1619] [PMID: 17632525]
[156]
Ladage D, Yaniz-Galende E, Rapti K, et al. Stimulating myocardial regeneration with periostin Peptide in large mammals improves function post-myocardial infarction but increases myocardial fibrosis. PLoS One 2013; 8(5)e59656
[http://dx.doi.org/10.1371/journal.pone.0059656] [PMID: 23700403]
[157]
Sawyer AJ, Kyriakides TR. Matricellular proteins in drug delivery: Therapeutic targets, active agents, and therapeutic localization. Adv Drug Deliv Rev 2016; 97: 56-68.
[http://dx.doi.org/10.1016/j.addr.2015.12.016] [PMID: 26763408]
[158]
Clifford DM, Fisher SA, Brunskill SJ, et al. Stem cell treatment for acute myocardial infarction. Cochrane Database Syst Rev 2012; 2(2)CD006536
[http://dx.doi.org/10.1002/14651858.CD006536.pub3] [PMID: 22336818]
[159]
Jang J, Park HJ, Kim SW, et al. 3D printed complex tissue construct using stem cell-laden decellularized extracellular matrix bioinks for cardiac repair. Biomaterials 2017; 112: 264-74.
[http://dx.doi.org/10.1016/j.biomaterials.2016.10.026] [PMID: 27770630]
[160]
Gaetani R, Feyen DA, Verhage V, et al. Epicardial application of cardiac progenitor cells in a 3D-printed gelatin/hyaluronic acid patch preserves cardiac function after myocardial infarction. Biomaterials 2015; 61: 339-48.
[http://dx.doi.org/10.1016/j.biomaterials.2015.05.005] [PMID: 26043062]
[161]
Guyette JP, Charest JM, Mills RW, et al. Bioengineering human myocardium on native extracellular matrix. Circ Res 2016; 118(1): 56-72.
[http://dx.doi.org/10.1161/CIRCRESAHA.115.306874] [PMID: 26503464]

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