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Cardiac muscle cell apoptosis is a highly regulated form of programmed cell death occurring in cardiomyocytes, driven by both intrinsic (mitochondrial) and extrinsic (death receptor-mediated) pathways. Key molecular executors include initiator caspases (e.g., caspase 8, 9), effector caspases (e.g., caspase 3, 7), and regulatory Bcl-2-family proteins (pro-apoptotic Bax, Bak; anti-apoptotic Bcl-2, Bcl-xL). This process is implicated in cardiac remodeling and is thought to contribute causally to progression of heart failure and other cardiac diseases. While apoptosis is not in itself a direct drug target, therapies may modulate upstream signaling pathways to protect cardiac muscle cells from excessive apoptotic loss
Drugs may modulate signaling pathways that regulate pro- and anti-apoptotic molecules, influence oxidative stress, block death receptors, or inhibit caspases
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