Hydrogen sulfide and ischemia–reperfusion injury

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 (H 2S). H 2S is the latest gasotransmitter to be identified and characterized and like the other members of the gasotransmitter family, H 2S 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, H 2S has gained much attention as a physiological signaling molecule. Also, much like NO and CO, H 2S's role in ischemia/reperfusion (I/R) injury has recently begun to be elucidated. As such, modulation of endogenous H 2S and administration of exogenous H 2S 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 H 2S plays in different model systems of I/R injury and will also detail some of the mechanisms involved with its cytoprotection.