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"Anti-apoptosis of ischemic myocardial cells" refers to a therapeutic strategy or biological process rather than a single molecular target. It encompasses the physiological and pharmacological efforts to prevent programmed cell death in heart muscle cells (cardiomyocytes) following a myocardial infarction or ischemia-reperfusion injury (PMID: 15310694). This process is critical because cardiomyocytes have limited regenerative capacity; their loss directly leads to ventricular remodeling and eventual heart failure. The signaling network involved includes the intrinsic (mitochondrial) pathway regulated by the Bcl-2 family and the extrinsic (death receptor) pathway (PMID: 21873606). Most drugs targeting this process aim to activate survival kinases like Akt or ERK1/2, or inhibit downstream executioner proteins like Caspase-3 to preserve cardiac function and reduce infarct size.
Activation of pro-survival pathways such as PI3K/Akt or JAK/STAT, and inhibition of pro-apoptotic proteins like Bax and Caspases to prevent cardiomyocyte loss.
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