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John W. Calvert

Researcher at Emory University

Publications -  126
Citations -  10346

John W. Calvert is an academic researcher from Emory University. The author has contributed to research in topics: Reperfusion injury & Cardioprotection. The author has an hindex of 49, co-authored 119 publications receiving 9261 citations. Previous affiliations of John W. Calvert include Yeshiva University & University of Mississippi Medical Center.

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Hydrogen sulfide attenuates myocardial ischemia-reperfusion injury by preservation of mitochondrial function

TL;DR: It is demonstrated that the delivery of H2S at the time of reperfusion limits infarct size and preserves left ventricular (LV) function in an in vivo model of myocardial ischemia-reperfusion (MI-R) and that either administration of H 2S or the modulation of endogenous production may be of clinical benefit in ischemic disorders.
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Hydrogen Sulfide Mediates Cardioprotection Through Nrf2 Signaling

TL;DR: Results reveal that the cardioprotective effects of H2S are mediated in large part by a combination of antioxidant and antiapoptotic signaling.
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Nitrite augments tolerance to ischemia/reperfusion injury via the modulation of mitochondrial electron transfer

TL;DR: It is reported that both acute and delayed exposure to physiological concentrations of nitrite, given both systemically or orally, potently limits cardiac and hepatic reperfusion injury and may represent an effector of the cell-survival program of ischemic preconditioning and the Mediterranean diet.
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Acute Metformin Therapy Confers Cardioprotection Against Myocardial Infarction Via AMPK-eNOS–Mediated Signaling

TL;DR: These findings provide important information that myocardial AMPK activation by metformin following I/R sets into motion events, including eNOS activation, which ultimately lead to cardioprotection.
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Activation of AMP-Activated Protein Kinase by Metformin Improves Left Ventricular Function and Survival in Heart Failure

TL;DR: It is demonstrated that metformin significantly improves left ventricular function and survival via activation of AMPK and its downstream mediators, eNOS and PGC-1&agr;, in a murine model of heart failure.