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

John W. Elrod, John W. Calvert, Joanna Morrison, Jeannette E. Doeller, David W. Kraus, Ling Tao, Xiangying Jiao, Rosario Scalia, Levente Kiss, Csaba Szabo, Hideo Kimura, Chi Wing Chow, David J. Lefer

    Research output: Contribution to journalArticlepeer-review

    818 Scopus citations


    The recent discovery that hydrogen sulfide (H2S) is an endogenously produced gaseous second messenger capable of modulating many physiological processes, much like nitric oxide, prompted us to investigate the potential of H2S as a cardioprotective agent. In the current study, we demonstrate 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). This observed cytoprotection is associated with an inhibition of myocardial inflammation and a preservation of both mitochondrial structure and function after I-R injury. Additionally, we show that modulation of endogenously produced H2S by cardiac-specific overexpression of cystathionine γ-lyase (α-MHC-CGL-Tg mouse) significantly limits the extent of injury. These findings demonstrate that H2S may be of value in cytoprotection during the evolution of myocardial infarction and that either administration of H2S or the modulation of endogenous production may be of clinical benefit in ischemic disorders.

    Original languageEnglish (US)
    Pages (from-to)15560-15565
    Number of pages6
    JournalProceedings of the National Academy of Sciences of the United States of America
    Issue number39
    StatePublished - Sep 25 2007

    ASJC Scopus subject areas

    • General

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