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Calpain system and its involvement in myocardial ischemia and reperfusion injury.

Abstract
Calpains are ubiquitous non-lysosomal Ca(2+)-dependent cysteine proteases also present in myocardial cytosol and mitochondria. Numerous experimental studies reveal an essential role of the calpain system in myocardial injury during ischemia, reperfusion and postischemic structural remodelling. The increasing Ca(2+)-content and Ca(2+)-overload in myocardial cytosol and mitochondria during ischemia and reperfusion causes an activation of calpains. Upon activation they are able to injure the contractile apparatus and impair the energy production by cleaving structural and functional proteins of myocytes and mitochondria. Besides their causal involvement in acute myocardial dysfunction they are also involved in structural remodelling after myocardial infarction by the generation and release of proapoptotic factors from mitochondria. Calpain inhibition can prevent or attenuate myocardial injury during ischemia, reperfusion, and in later stages of myocardial infarction.
AuthorsChristiane Neuhof, Heinz Neuhof
JournalWorld journal of cardiology (World J Cardiol) Vol. 6 Issue 7 Pg. 638-52 (Jul 26 2014) ISSN: 1949-8462 [Print] United States
PMID25068024 (Publication Type: Journal Article, Review)

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