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• W2037210083 endingPage "426" @default.
• W2037210083 startingPage "412" @default.
• W2037210083 abstract "A bstract : The signal transduction pathways by which ischemia‐reperfusion leads to apoptosis may involve the JNK pathway, ceramide generation, and inhibition of protective PKC pathways. The biochemical events associated with apoptosis include mitochondrial inactivation, cytochrome c dislocation, caspase activation, and cytoplasmic acidification. Through the concerted efforts of multiple classes of enzymes, apoptosis is accomplished, resulting in the death of a cell in which potentially transforming oncogenes have been degraded and inflammatory contents are contained within the plasma membrane until the fragments can be ingested by phagocytes. This non‐inflammatory mode of cell death permits tissue remodeling with minimal scar formation, and so is preferable to necrotic cell death. The distinction between apoptosis and necrosis, which implies different mechanisms of cell death, is blurred in the case of a pathologic insult such as ischemia‐reperfusion. It is suggested that it is more useful to view cell death in the context of whether or not it can be prevented" @default.
• W2037210083 created "2016-06-24" @default.
• W2037210083 creator A5017792849 @default.
• W2037210083 creator A5049533029 @default.
• W2037210083 date "1999-06-01" @default.
• W2037210083 modified "2023-10-13" @default.
• W2037210083 title "Apoptosis in Myocardial Ischemia‐Reperfusion" @default.
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• W2037210083 doi "https://doi.org/10.1111/j.1749-6632.1999.tb09255.x" @default.
• W2037210083 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/10415551" @default.
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