Protective Actions of H2S in Acute Myocardial Infarction and Heart Failure.
Hydrogen sulfide (H2S) was identified as the third gasotransmitter in 1996 following the discoveries of the biological importance of nitric oxide and carbon monoxide. Although H2S has long been considered a highly toxic gas, the discovery of its presence and enzymatic production in mammalian tissues supports a critical role for this physiological signaling molecule. H2S is synthesized endogenously by three enzymes: cystathionine β-synthase, cystathionine-γ-lyase, and 3-mercaptopyruvate sulfurtransferase. H2S plays a pivotal role in the regulation of cardiovascular function as H2S has been shown to modulate: vasodilation, angiogenesis, inflammation, oxidative stress, and apoptosis. Perturbation of endogenous production of H2S has been associated with many pathological conditions of the cardiovascular system such as diabetes, heart failure, and hypertension. As such, modulation of the endogenous H2S signaling pathway or administration of exogenous H2S has been shown to be cytoprotective. This review article will provide a summary of the current body of evidence on the role of H2S signaling in the setting of myocardial ischemia and heart failure. © 2017 American Physiological Society. Compr Physiol 7:583-602, 2017.
Cardiovascular Center of Excellence Louisiana State University Health Sciences Center, New Orleans, Louisiana, USA.
Erminia
E
Donnarumma
Cardiovascular Center of Excellence Louisiana State University Health Sciences Center, New Orleans, Louisiana, USA.
Rishi K
RK
Trivedi
Cardiovascular Center of Excellence Louisiana State University Health Sciences Center, New Orleans, Louisiana, USA.
David J
DJ
Lefer
D000208:Acute Disease; D000818:Animals; D002316:Cardiotonic Agents / Q000494:pharmacology / Q000627:therapeutic use; D006333:Heart Failure / Q000503:physiopathology / Q000517:prevention & control*; D006801:Humans; D006862:Hydrogen Sulfide / Q000737:chemistry / Q000378:metabolism / Q000494:pharmacology / Q000627:therapeutic use*; D008928:Mitochondria / Q000187:drug effects / Q000378:metabolism; D009203:Myocardial Infarction / Q000503:physiopathology / Q000517:prevention & control*; D018384:Oxidative Stress / Q000187:drug effects / Q000502:physiology; D015221:Potassium Channels / Q000187:drug effects / Q000502:physiology
D002316:Cardiotonic Agents; D015221:Potassium Channels; D006862:Hydrogen Sulfide