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Author Notes:
Correspondence: John W. Calvert, Ph.D., Department of Surgery, Division of Cardiothoracic Surgery, Emory University School of Medicine, 550 Peachtree Street NE, Atlanta, GA 30308; Phone: 404-686-1832; Email: jcalver@emory.edu
Disclosures: Authors have no disclosures.
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Research Funding:
Supported by grants from the American Diabetes Association (7-09-BS-26) and the National Institutes of Health National Heart Lung and Blood Institute (NHLBI) 1R01HL098481-01 to J.W.C.
This work was also supported by funding from the Carlyle Fraser Heart Center (CFHC) of Emory University Hospital Midtown.
Hydrogen Sulfide and Ischemia - Reperfusion Injury
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Abstract:
Gasotransmitters are lipid soluble, endogenously produced gaseous signaling molecules that freely permeate the plasma membrane of a cell to directly activate intracellular targets, thus alleviating the need for membrane-bound receptors. The gasotransmitter family consists of three members: nitric oxide (NO), carbon monoxide (CO), and hydrogen sulfide (H2S). H2S is the latest gasotransmitter to be identified and characterized and like the other members of the gasotransmitter family, H2S was historically considered to be a toxic gas and an environmental/occupational hazard. However with the discovery of its presence and enzymatic production in mammalian tissues, H2S has gained much attention as a physiological signaling molecule. Also, much like NO and CO, H2S’s role in ischemia/reperfusion (I/R) injury has recently begun to be elucidated. As such, modulation of endogenous H2S and administration of exogenous H2S has now been demonstrated to be cytoprotective in various organ systems through diverse signaling mechanisms. This review will provide a detailed description of the role H2S plays in different model systems of I/R injury and will also detail some of the mechanisms involved with its cytoprotection.
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© 2010 Elsevier Ltd. All rights reserved.
This is an Open Access work distributed under the terms of the Creative Commons Attribution-NonCommerical-NoDerivs 3.0 Unported License (http://creativecommons.org/licenses/by-nc-nd/3.0/).
