Hydrogen sulfide attenuates myocardial ischemia-reperfusion injury by preservation of mitochondrial function
By J. Elrod, J. Calvert, J. Morrison, J. Doeller, D. Kraus, L. Tao, X. Jiao, R. Scalia, L. Kiss, C. Szabó and 3 more. Proceedings of the National Academy of Sciences of the United States of America, 2007
1,110 citations recorded by the source corpus.
Subfields: Biochemistry, Physiology
View Paper: https://www.semanticscholar.org/paper/2a7299793845c74632b9ba5aa3b8af2a602afe49
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Citations in the corpus
- H2S ameliorates oxidative and proteolytic stresses and protects the heart against adverse remodeling in chronic heart failure. (2010, result): “These findings extended concrete support to other findings that H2S is a cardioprotective gas (3, 4, 8).”
- Hydrogen sulfide is an endogenous stimulator of angiogenesis (2009, background): “In animal models of critical illness, H2S donors protect from lethal hypoxia and reperfusion injury (3, 8, 9) and exert anti-inflammatory effects (10).”
- Physiological implications of hydrogen sulfide: a whiff exploration that blossomed. (2012, background): “(160) demonstrated that cardiacspecific overexpression of CSE significantly limits mouse cardiac ischemia-reperfusion damage due to increased endogenous level.”
- Hydrogen Sulfide Increases Glutathione Production and Suppresses Oxidative Stress in Mitochondria (2010, positive): “In addition to neurons, H2S protects cardiac muscle from myocardial ischemia=reperfusion injury by preserving mitochondrial function (16, 50).”
- Protective Actions of H2S in Acute Myocardial Infarction and Heart Failure (2017, positive): “Experimental evidence have shown that a bolus of Na 2 S, administered at dosage of 50 μ g/kg given at time of reperfusion or 100 μ g/kg at 24 h prior to the ischemic event, reduces the infarct size by 72% and 46%, respectively (22,42).”
- Hydrogen Sulfide Mediates Cardioprotection Through Nrf2 Signaling (2009, methodology): “Three different stains of mice were utilized: (1) Male C57BL6/J mice, 8-”
- Redox chemistry of biological thiols (2010, background): “inflammatory events and ischemia reperfusion injury [216].”