Reduction of Ischemia/Reperfusion Injury With Bendavia, a Mitochondria‐Targeting Cytoprotective Peptide

Background Manifestations of reperfusion injury include myocyte death leading to infarction, contractile dysfunction, and vascular injury characterized by the “no‐reflow” phenomenon. Mitochondria‐produced reactive oxygen species are believed to be centrally involved in each of these aspects of reper...

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Bibliographic Details
Published in:Journal of the American Heart Association 2012-06, Vol.1 (3), p.e001644-n/a
Main Authors: Kloner, Robert A., Hale, Sharon L., Dai, Wangde, Gorman, Robert C., Shuto, Takashi, Koomalsingh, Kevin J., Gorman, Joseph H., Sloan, Ruben C., Frasier, Chad R., Watson, Corinne A., Bostian, Phillip A., Kypson, Alan P., Brown, David A.
Format: Article
Language:English
Subjects:
cardioprotection
infarction
mitochondria
Original Research
peptide
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Summary:Background Manifestations of reperfusion injury include myocyte death leading to infarction, contractile dysfunction, and vascular injury characterized by the “no‐reflow” phenomenon. Mitochondria‐produced reactive oxygen species are believed to be centrally involved in each of these aspects of reperfusion injury, although currently no therapies reduce reperfusion injury by targeting mitochondria specifically. Methods and Results We investigated the cardioprotective effects of a mitochondria‐targeted peptide, Bendavia (Stealth Peptides), across a spectrum of experimental cardiac ischemia/reperfusion models. Postischemic administration of Bendavia reduced infarct size in an in vivo sheep model by 15% (P=0.02) and in an ex vivo guinea pig model by 38% to 42% (P
ISSN:2047-9980
2047-9980
DOI:10.1161/JAHA.112.001644