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Hydrogen sulfide attenuates myocardial ischemia-reperfusion injury by preservation of mitochondrial function
Open accessAbstract
The recent discovery that hydrogen sulfide (H 2 S) is an endogenously produced gaseous second messenger capable of modulating many physiological processes, much like nitric oxide, prompted us to investigate the potential of H 2 S as a cardioprotective agent. In the current study, we demonstrate that the delivery of H 2 S 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 H 2 S by cardiac-specific overexpression of cystathionine γ-lyase (α-MHC-CGL-Tg mouse) significantly limits the extent of injury. These findings demonstrate that H 2 S may be of value in cytoprotection during the evolution of myocardial infarction and that either administration of H 2 S or the modulation of endogenous production may be of clinical benefit in ischemic disorders.
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Metadata
- Authors
- Elrod, J. W., Calvert, J. W., Morrison, J., Doeller, J. E., Kraus, D. W., Tao, L., Jiao, X., Scalia, R., Kiss, L., Szabo, C., Kimura, H., Chow, C.-W., & Lefer, D. J.
- Venue
- Proceedings of the National Academy of Sciences
- Published
- 2007-09-25
- Volume
- 104
- Issue
- 39
- Pages
- 15560-15565
- ISSN
- 0027-8424 (ISSN-L)
- 1091-6490
- OpenAlex
- W2169746496
- Cited by
- 1,255
- References
- 2
- FWCI
- 63.81
- Type
- journal article
- Language
- en
- Open access
- green
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