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, L. Kiss, Csaba Szabo, Hideo Kimura, Chi Wing Chow, David J. Lefer

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718 Citations (Scopus)

Abstract

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
Pages (from-to)15560-15565
Number of pages6
JournalProceedings of the National Academy of Sciences of the United States of America
Volume104
Issue number39
DOIs
Publication statusPublished - Sep 25 2007

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Myocardial Reperfusion Injury
Hydrogen Sulfide
Cytoprotection
Reperfusion Injury
Myocardial Ischemia
Cystathionine
Physiological Phenomena
Cardiotonic Agents
Myocardial Reperfusion
Lyases
Wounds and Injuries
Second Messenger Systems
Left Ventricular Function
Reperfusion
Nitric Oxide
Myocardial Infarction
Inflammation

ASJC Scopus subject areas

  • Genetics
  • General

Cite this

Hydrogen sulfide attenuates myocardial ischemia-reperfusion injury by preservation of mitochondrial function. / Elrod, John W.; Calvert, John W.; Morrison, Joanna; Doeller, Jeannette E.; Kraus, David W.; Tao, Ling; Jiao, Xiangying; Scalia, Rosario; Kiss, L.; Szabo, Csaba; Kimura, Hideo; Chow, Chi Wing; Lefer, David J.

In: Proceedings of the National Academy of Sciences of the United States of America, Vol. 104, No. 39, 25.09.2007, p. 15560-15565.

Research output: Contribution to journalArticle

Elrod, JW, Calvert, JW, Morrison, J, Doeller, JE, Kraus, DW, Tao, L, Jiao, X, Scalia, R, Kiss, L, Szabo, C, Kimura, H, Chow, CW & Lefer, DJ 2007, 'Hydrogen sulfide attenuates myocardial ischemia-reperfusion injury by preservation of mitochondrial function', Proceedings of the National Academy of Sciences of the United States of America, vol. 104, no. 39, pp. 15560-15565. https://doi.org/10.1073/pnas.0705891104
Elrod, John W. ; Calvert, John W. ; Morrison, Joanna ; Doeller, Jeannette E. ; Kraus, David W. ; Tao, Ling ; Jiao, Xiangying ; Scalia, Rosario ; Kiss, L. ; Szabo, Csaba ; Kimura, Hideo ; Chow, Chi Wing ; Lefer, David J. / Hydrogen sulfide attenuates myocardial ischemia-reperfusion injury by preservation of mitochondrial function. In: Proceedings of the National Academy of Sciences of the United States of America. 2007 ; Vol. 104, No. 39. pp. 15560-15565.
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