Regulation of cardiovascular cell function by hydrogen sulfide (H2S)
- 26 January 2010
- journal article
- review article
- Published by Wiley in Cell Biochemistry and Function
- Vol. 28 (2), 95-106
- https://doi.org/10.1002/cbf.1618
Abstract
Since the discovery of endogenously‐produced hydrogen sulfide (H2S) in various tissues, there has been an explosion of interest in H2S as a biological mediator alongside other gaseous mediators, nitric oxide and carbon monoxide. The identification of enzyme‐regulated H2S synthetic pathways in the cardiovascular system has led to a number of studies examining specific regulatory actions of H2S. We review evidence showing that endogenously‐generated and exogenously‐administered H2S exerts a wide range of actions in vascular and myocardial cells including vasodilator/vasoconstrictor effects via modification of the smooth muscle tone, induction of apoptosis and anti‐proliferative responses in the smooth muscle cells, angiogenic actions, effects relevant to inflammation and shock, and cytoprotection in models of myocardial ischemia‐reperfusion injury. Several molecular mechanisms of action of H2S have been described. These include interactions of H2S with NO, redox regulation of multiple signaling proteins and regulation of KATP channel opening. The gaps in our current understanding of precise mechanisms, the absence of selective pharmacological tools and the limited availability of H2S measurement techniques for living tissues, leave many questions about physiological and pathophysiological roles of H2S unanswered at present. Nevertheless, this area of investigation is advancing rapidly. We believe H2S holds promise as an endogenous mediator controlling a wide range of cardiovascular cell functions and integrated responses under both physiological and pathological conditions and may be amenable to therapeutic manipulation. Copyright © 2010 John Wiley & Sons, Ltd.This publication has 82 references indexed in Scilit:
- The effects of therapeutic sulfide on myocardial apoptosis in response to ischemia–reperfusion injury☆☆☆European Journal of Cardio-Thoracic Surgery, 2008
- The hydrogen sulphide-releasing derivative of diclofenac protects against ischaemia-reperfusion injury in the isolated rabbit heartBritish Journal of Pharmacology, 2008
- Hydrogen sulfide attenuates myocardial ischemia-reperfusion injury by preservation of mitochondrial functionProceedings of the National Academy of Sciences of the United States of America, 2007
- Protective Effect of Hydrogen Sulfide on Balloon Injury-Induced Neointima Hyperplasia in Rat Carotid ArteriesThe American Journal of Pathology, 2007
- Anti-inflammatory and gastrointestinal effects of a novel diclofenac derivativeFree Radical Biology & Medicine, 2007
- Regulation of vascular nitric oxide in vitro and in vivo; a new role for endogenous hydrogen sulphide?British Journal of Pharmacology, 2006
- Hydrogen sulfide is an endogenous modulator of leukocyte‐mediated inflammationThe FASEB Journal, 2006
- Hydrogen sulfide inhibits nitric oxide production and nuclear factor-κB via heme oxygenase-1 expression in RAW264.7 macrophages stimulated with lipopolysaccharideFree Radical Biology & Medicine, 2006
- Impact of hydrogen sulfide on carbon monoxide/heme oxygenase pathway in the pathogenesis of hypoxic pulmonary hypertensionBiochemical and Biophysical Research Communications, 2004
- The vasorelaxant effect of H2S as a novel endogenous gaseous KATP channel openerThe EMBO Journal, 2001