For more than a century, hydrogen sulfide (H2S) has been regarded as a toxic gas. This review surveys the growing recognition of the role of H2S as an endogenous signaling molecule in mammals, with emphasis on its physiological and pathological pathways in the cardiovascular system. In biological fluids, H2S gas is a weak acid that exists as about 15% H2S, 85% HS−, and a trace of S2−. Here, we use “H2S” to refer to this mixture. H2S has been found to influence heart contractile functions and may serve as a cardioprotectant for treating ischemic heart diseases and heart failure. Alterations of the endogenous H2S level have been found in animal models with various pathological conditions such as myocardial ischemia, spontaneous hypertension, and hypoxic pulmonary hypertension. In the vascular system, H2S exerts biphasic regulation of a vascular tone with varying effects based on its concentration and in the presence of nitric oxide. Over the past decade, several H2S-releasing compounds (NaHS, Na2S, GYY4137, etc.) have been utilized to test the effect of exogenous H2S under different physiological and pathological situations in vivo and in vitro. H2S has been found to promote angiogenesis and to protect against atherosclerosis and hypertension, while excess H2S may promote inflammation in septic or hemorrhagic shock. H2S-releasing compounds and inhibitors of H2S synthesis hold promise in alleviating specific disease conditions. This comprehensive review covers in detail the effects of H2S on the cardiovascular system, especially in disease situations, and also the various underlying mechanisms. Antioxid. Redox Signal. 17, 141–185.
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