索引超出了数组界限。
[1] Weber KT, Brilla CG. Pathological hypertrophy and cardiac interstitium. Fibrosis and renin-angiotensin-aldosterone system [J]. Circulation,1991,83(6):1849-1865.
[2] Balakumar P, Singh AP, Singh M. Rodent models of heart failure[J]. J Pharmacol Toxicol Methods,2007,56(1):1-10.
[3] Sundstrom J, Sullivan L, Selhub J, et al. Relations of plasma homocysteine to left ventricular structure and function: the Framingham Heart Study[J]. Eur Heart J,2004,25(6):523-530.
[4] Nasir K, Tsai M, Rosen BD, et al. Elevated homocysteine is associated with reduced regional left ventricular function the multi-ethnic study of atherosclerosis[J]. Circulation,2007,115(2):180-187.
[5] Ruhui L, Jinfa J, Jiahong X, et al. Influence of hyperhomocysteinemia on left ventricular diastolic function in Chinese patients with hypertension[J]. Herz,2015,40(4):679-684.
[6] Washio T, Nomoto K, Watanabe I, et al. Relationship between Plasma homocysteine levels and congestive heart failure in patients with acute myocardial infarction homocysteine and congestive heart failure[J]. Int Heart J,2011,52(4):224-228.
[7] Vasan RS, Beiser A, D'agostino RB, et al. Plasma homocysteine and risk for congestive heart failure in adults without prior myocardial infarction[J]. JAMA,2003,289(10):1251-1257.
[8] Okuyan E, Uslu A, Akar MA, et al. Homocysteine levels in patients with heart failure with preserved ejection fraction[J]. Cardiology,2010,117(1):21-27.
[9] Wang X, Cui L, Joseph J, et al. Homocysteine induces cardiomyocyte dysfunction and apoptosis through p38 MAPK-mediated increase in oxidant stress[J]. J Mol Cell Cardiol,2012,52(3):753-760.
[10] Moshal KS, Tipparaju SM, Vacek TP, et al. Mitochondrial matrix metalloproteinase activation decreases myocyte contractility in hyperhomocysteinemia[J]. Am J Physiol Heart Circ Physiol,2008,295(2):H890-H897.
[11] Ma S, Zhang H, Sun W, et al. Hyperhomocysteinemia induces cardiac injury by up-regulation of p53-dependent Noxa and Bax expression through the p53 DNA methylation in ApoE-/- mice[J]. Acta Bioch Bioph Sin,2013,45(5):391-400.
[12] Muthuramu I, Singh N, Amin R, et al. Selective homocysteine-lowering gene transfer attenuates pressure overload-induced cardiomyopathy via reduced oxidative stress[J]. J Mol Med(Berl),2015,93(6):609-618.
[13] Muthuramu I, Jacobs F, Singh N, et al. Selective homocysteine lowering gene transfer improves infarct healing, attenuates remodelling, and enhances diastolic function after myocardial infarction in mice[J]. PLoS One,2013,8(5):e63710.
[14] Loscalzo J. The oxidant stress of hyperhomocyst(e)inemia[J]. J Clin Invest,1996,98(1):5-7.
[15] Tyagi N, Sedoris KC, Steed M, et al. Mechanisms of homocysteine-induced oxidative stress[J]. Am J Physiol Heart Circ Physiol,2005,289(6):H2649-H2656.
[16] Martinez E, Gérard N, Garcia MM, et al. Myocardium proteome remodelling after nutritional deprivation of methyl donors[J]. J Nutr Biochem,2013,24(7):1241-1250.
[17] Mcdowell IF,Lang D. Homocysteine and endothelial dysfunction: a link with cardiovascular disease[J]. J Nutr,2000,130(2s Suppl):369S-372S.
[18] Sood HS, Cox MJ, Tyagi SC. Generation of nitrotyrosine precedes activation of metalloproteinase in myocardium of hyperhomocysteinemic rats[J]. Antioxid Redox Signal,2002,4(5):799-804.
[19] Wollert KC, Fiedler B, Gambaryan S, et al. Gene transfer of cGMP-dependent protein kinase I enhances the antihypertrophic effects of nitric oxide in cardiomyocytes[J]. Hypertension, 2002, 39(1):87-92.
[20] Kundu S, Kumar M, Sen U, et al. Nitrotyrosinylation, remodeling and endothelial‐myocyte uncoupling in iNOS, cystathionine beta synthase(CBS)knockouts and iNOS/CBS double knockout mice[J]. J Cell Biochem,2009,106(1):119-126.
[21] Suematsu N, Ojaimi C, Kinugawa S, et al. Hyperhomocysteinemia alters cardiac substrate metabolism by impairing nitric oxide bioavailability through oxidative stress[J]. Circulation,2007,115(2):255-262.
[22] Recchia FA, Mcconnell PI, Bernstein RD, et al. Reduced nitric oxide production and altered myocardial metabolism during the decompensation of pacing-induced heart failure in the conscious dog[J]. Circ Res,1998,83(10):969-979.
[23] Joseph J, Joseph L, Devi S, et al. Effect of anti-oxidant treatment on hyperhomocysteinemia-induced myocardial fibrosis and diastolic dysfunction[J]. J Heart Lung Transpl, 2008,27(11):1237-1241.
[24] Torre-Amione G, Kapadia S, Lee J, et al. Tumor necrosis factor-α and tumor necrosis factor receptors in the failing human heart[J]. Circulation,1996,93(4):704-711.
[25] Raaf L, Noll C, Cherifi Mel H, et al. Myocardial fibrosis and TGFB expression in hyperhomocysteinemic rats[J]. Mol Cell Biochem,2011,347(1-2):63-70.
[26] Singh AP, Singh M, Balakumar P. Effect of mast cell stabilizers in hyperhomocysteinemia-induced cardiac hypertrophy in rats[J]. J Cardiovasc Pharm,2008,51(6):596-604.
[27] Pang X, Liu J, Zhao J, et al. Homocysteine induces the expression of C-reactive protein via NMDAr-ROS-MAPK-NF-κB signal pathway in rat vascular smooth muscle cells[J]. Atherosclerosis,2014,236(1):73-81.
[28] Swindle EJ, Metcalfe DD,Coleman JW. Rodent and human mast cells produce functionally significant intracellular reactive oxygen species but not nitric oxide[J]. J Biol Chem,2004,279(47):48751-48759.
[29] Tyagi SC, Ratajska A, Weber KT. Myocardial matrix metalloproteinase(s): localization and activation[J]. Mol Cell Biochem,1993,126(1):49-59.
[30] Henderson BC,Tyagi SC. Oxidative mechanism and homeostasis of proteinase/antiproteinase in congestive heart failure[J]. J Mol Cell Cardiol,2006,41(6):959-962.
[31] Herrmann W, Herrmann M, Joseph J, et al. Homocysteine, brain natriuretic peptide and chronic heart failure: a critical review[J]. Clin Chem Lab Med,2007,45(12):1633-1644.
[32] Krainc D, Bai G, Okamoto S, et al. Synergistic Activation of theN-Methyl-D-aspartate Receptor Subunit 1 Promoter by Myocyte Enhancer Factor 2C and Sp1[J]. J Biol Chem,1998,273(40):26218-26224.
[33] Folbergrová J. NMDA and not non-NMDA receptor antagonists are protective against seizures induced by homocysteine in neonatal rats[J]. Eex Neurol,1994,130(2):344-350.
[34] Moshal KS, Metreveli N, Frank I, et al. Mitochondrial MMP activation, dysfunction and arrhythmogenesis in hyperhomocysteinemia[J]. Curr Vasc Pharmacol,2008,6(2):84-92.
[35] Moshal KS, Kumar M, Tyagi N, et al. Restoration of contractility in hyperhomocysteinemia by cardiac-specific deletion of NMDA-R1[J]. Am J Physiol-heart C,2009,296(3):H887-H892.
[36] Chaturvedi P, Kalani A, Givvimani S, et al. Differential regulation of DNA methylation versus histone acetylation in cardiomyocytes during HHcy in vitro and in vivo: an epigenetic mechanism[J]. Phsiol Genomics,2014,46(7):245-255.
[37] Jiang Y, Sun T, Xiong J, et al. Hyperhomocysteinemia‐mediated DNA Hypomethylation and its Potential Epigenetic Role in Rats[J]. Acta Biochim Bioph Sin,2007,39(9):657-667.
[38] Garcia MM, Guéant-Rodriguez RM, Pooya S, et al. Methyl donor deficiency induces cardiomyopathy through altered methylation/acetylation of PGC-1α by PRMT1 and SIRT1[J]. J Pathol,2011,225(3):324-335.
[39] Mani S, Li H, Untereiner A, et al. Decreased endogenous production of hydrogen sulfide accelerates atherosclerosis[J]. Circulation,2013,127(25):2523-2534.
[40] Chen P, Poddar R, Tipa EV, et al. Homocysteine metabolism in cardiovascular cells and tissues: implications for hyperhomocysteinemia and cardiovascular disease[J]. Adv Enzyme Regul,1999,39:93-109.
[41] Kesherwani V, Nandi SS, Sharawat SK, et al. Hydrogen sulfide mitigates homocysteine-mediated pathological remodeling by inducing miR-133a in cardiomyocytes[J]. Mol Cell Biochem,2015,404(1-2):241-250.
[42] Martí-Carvajal AJ, Solà I, Lathyris D. Homocysteine‐lowering interventions for preventing cardiovascular events[J]. Cochrane Database Syst Rev,2015,1:CD006612.