The Cardioprotective Effects of Hydrogen Sulfide in Heart Diseases: From Molecular Mechanisms to Therapeutic Potential

Oxidative Medicine and Cellular Longevity - Tập 2015 - Trang 1-13 - 2015
Yaqi Shen1,2, Zhuqing Shen1, Shanshan Luo1, Wei Guo1, Yi Zhun Zhu3,1
1Department of Pharmacology, School of Pharmacy, Fudan University, Zhangheng Road 826, Pudong New District, Shanghai 201203, China
2Department of Physiology and Pathophysiology, Shanghai Medical college, Fudan University, Shanghai 200032, China
3Department of Pharmacology, National University of Singapore, Singapore 117597

Tóm tắt

Hydrogen sulfide (H2S) is now recognized as a third gaseous mediator along with nitric oxide (NO) and carbon monoxide (CO), though it was originally considered as a malodorous and toxic gas. H2S is produced endogenously from cysteine by three enzymes in mammalian tissues. An increasing body of evidence suggests the involvement of H2S in different physiological and pathological processes. Recent studies have shown that H2S has the potential to protect the heart against myocardial infarction, arrhythmia, hypertrophy, fibrosis, ischemia-reperfusion injury, and heart failure. Some mechanisms, such as antioxidative action, preservation of mitochondrial function, reduction of apoptosis, anti-inflammatory responses, angiogenic actions, regulation of ion channel, and interaction with NO, could be responsible for the cardioprotective effect of H2S. Although several mechanisms have been identified, there is a need for further research to identify the specific molecular mechanism of cardioprotection in different cardiac diseases. Therefore, insight into the molecular mechanisms underlying H2S action in the heart may promote the understanding of pathophysiology of cardiac diseases and lead to new therapeutic targets based on modulation of H2S production.

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Tài liệu tham khảo

1996, The Journal of Neuroscience, 16, 1066, 10.1523/JNEUROSCI.16-03-01066.1996

10.1096/fj.02-0211hyp

10.1152/physrev.00017.2011

10.1211/jpp/61.02.0010

10.1186/cc7700

10.1089/ars.2008.2253

10.1126/science.1162667

10.1371/journal.pone.0021971

10.2337/db05-1082

10.1186/1477-7827-7-10

1982, Biochemical Journal, 206, 267, 10.1042/bj2060267

10.1006/bbrc.1997.6878

10.1113/jphysiol.2005.097642

10.1042/BJ20110841

10.1074/jbc.m111.298208

10.1093/jb/mvp111

10.1089/ars.2008.2253

10.1146/annurev-pharmtox-010510-100505

10.1042/cs20100462

10.1038/ncomms2371

10.3389/fphys.2012.00101

10.1016/j.neuint.2013.09.003

10.1016/0006-2952(80)90346-9

2005, Academic Journal of the First Medical College of PLA, 25, 951

10.1155/2014/768607

10.1089/ars.2011.4005

10.1016/S0008-6363(00)00078-X

10.1590/s0100-879x2012007500090

10.1016/j.niox.2013.04.008

10.1097/fjc.0b013e3181b2b72b

2012, Fiziolohichnyǐ Zhurnal, 58, 57, 10.15407/fz58.06.057

10.1248/bpb.32.1406

10.1073/pnas.0705891104

10.1006/jmcc.1996.0193

10.1007/s003950050195

10.1152/japplphysiol.00096.2006

10.1089/ars.2009.2947

2014, Antioxidants & Redox Signaling

10.7150/ijbs.3632

10.1620/tjem.226.29

10.2459/jcm.0b013e32832997f3

10.1139/y07-120

10.1124/jpet.105.092023

10.1038/nature06321

10.3892/mmr.2012.748

10.1016/j.yjmcc.2008.01.007

10.1210/en.2013-2011

10.1016/j.cardiores.2004.08.020

10.1152/ajpheart.00682.2009

10.1371/journal.pone.0007307

10.1111/jcmm.12114

10.1042/bsr20100003

10.1016/j.ijcard.2013.06.007

10.1161/01.cir.0000034047.70205.97

10.1007/s11010-013-1686-7

10.1161/atvbaha.112.300484

10.1007/s12013-014-0113-3

10.3892/mmr.2012.748

10.1371/journal.pone.0094228

10.1161/circulationaha.109.920991

10.1161/CIRCULATIONAHA.112.000855

2011, Circulation, 124

10.1161/CIRCHEARTFAILURE.113.000299

10.3109/13813455.2012.755548

2013, Biomedical Reports, 1, 454, 10.3892/br.2013.87

10.1089/ars.2012.4888

10.1371/journal.pone.0069205

10.1089/ars.2013.5449

10.1042/CS20080500

10.12980/apjtb.4.201414b58

10.1089/ars.2009.2956

10.3892/ijmm.2013.1462

10.1007/s11010-013-1946-6

10.1042/cs20140460

10.1152/ajpheart.00796.2012

10.1016/j.bbrc.2012.03.121

10.1038/nrd2425

10.1089/ars.2009.2882

10.1152/ajpcell.00282.2007

10.1042/bj20082421

10.1089/ars.2009.2695

10.1016/j.ejphar.2010.12.010

10.1016/j.bbadis.2005.06.008

10.1042/bst0351040

10.1146/annurev.physiol.69.031905.163645

10.1177/1535370213477989

10.1016/j.ejcts.2008.01.047

10.1152/ajpheart.00339.2009

10.1073/pnas.041611398

1994, Journal of Thoracic and Cardiovascular Surgery, 108, 626, 10.1016/S0022-5223(94)70286-1

10.1378/chest.118.2.503

10.1586/ecp.10.134

10.1016/j.jtcvs.2008.08.074

10.1096/fj.06-6270fje

10.1007/s00726-011-0834-1

10.1111/j.1476-5381.2010.01191.x

10.1073/pnas.0908047106

10.1152/japplphysiol.01064.2010

10.1093/emboj/20.21.6008

10.1089/ars.2011.3882

10.1089/ars.2012.4565

10.1146/annurev.physiol.70.113006.100455

10.1111/j.1440-1681.2010.05351.x

10.1093/cvr/cvn140

10.1371/journal.pone.0037073

10.1016/j.ceca.2006.04.025

10.1096/fj.14-257113

10.1124/mol.105.017467

2007, Biochemical and Biophysical Research Communications, 358, 1142, 10.1016/j.bbrc.2007.05.063

10.1007/s00395-005-0569-9

10.1139/y07-120

10.1152/ajpgi.00556.2010

10.4149/gpb_2009_02_190

10.1073/pnas.1321871111

10.1016/j.bbrc.2006.02.154

10.1152/ajpheart.00044.2012

2007, Pharmacological Reports, 59, 4

10.1007/s00059-013-4047-0

10.1371/journal.pone.0077047

10.1371/journal.pone.0113305

10.1016/j.bbrc.2011.08.101

10.1161/circgenetics.113.000381

10.1096/fj.04-1815fje

10.1021/jm901638j

10.1021/cb400090d

10.1152/ajpheart.00044.2012

10.1016/j.ijcard.2012.12.004

10.1002/mnfr.200900278

10.1152/ajpheart.00853.2007

10.1097/fjc.0b013e3181ac8e12

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Oxidative Medicine and Cellular Longevity

Tập 2015

1-13

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