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- W2153111539 endingPage "31" @default.
- W2153111539 startingPage "23" @default.
- W2153111539 abstract "Loss of calcium (Ca2+) homeostasis contributes through different mechanisms to cell death occurring during the first minutes of reperfusion. One of them is an unregulated activation of a variety of Ca2+-dependent enzymes, including the non-lysosomal cysteine proteases known as calpains. This review analyses the involvement of the calpain family in reperfusion-induced cardiomyocyte death. Calpains remain inactive before reperfusion due to the acidic pHi and increased ionic strength in the ischaemic myocardium. However, inappropriate calpain activation occurs during myocardial reperfusion, and subsequent proteolysis of a wide variety of proteins contributes to the development of contractile dysfunction and necrotic cell death by different mechanisms, including increased membrane fragility, further impairment of Na+ and Ca2+ handling, and mitochondrial dysfunction. Recent studies demonstrating that calpain inhibition contributes to the cardioprotective effects of preconditioning and postconditioning, and the beneficial effects obtained with new and more selective calpain inhibitors added at the onset of reperfusion, point to the potential cardioprotective value of therapeutic strategies designed to prevent calpain activation." @default.
- W2153111539 created "2016-06-24" @default.
- W2153111539 creator A5006099883 @default.
- W2153111539 creator A5012713403 @default.
- W2153111539 creator A5029887131 @default.
- W2153111539 date "2012-07-10" @default.
- W2153111539 modified "2023-10-10" @default.
- W2153111539 title "Contribution of calpains to myocardial ischaemia/reperfusion injury" @default.
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