The Cardioprotective Effects of Hydrogen Sulfide in Heart Diseases: From Molecular Mechanisms to Therapeutic PotentialReport as inadecuate

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Oxidative Medicine and Cellular Longevity - Volume 2015 2015, Article ID 925167, 13 pages -

Review Article

Department of Pharmacology, School of Pharmacy, Fudan University, Zhangheng Road 826, Pudong New District, Shanghai 201203, China

Department of Physiology and Pathophysiology, Shanghai Medical College, Fudan University, Shanghai 200032, China

Department of Pharmacology, National University of Singapore, Singapore 117597

Received 3 November 2014; Accepted 18 December 2014

Academic Editor: Steven S. An

Copyright © 2015 Yaqi Shen et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


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.

Author: Yaqi Shen, Zhuqing Shen, Shanshan Luo, Wei Guo, and Yi Zhun Zhu



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