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The caspase apoptotic pathway comprises a family of cysteine-dependent aspartate-specific proteases (caspases) that execute programmed cell death (apoptosis) via a highly regulated proteolytic cascade[3][1][7][5]. There are initiator caspases (e.g., caspase-8, -9, -10) activated by extrinsic signals (death receptors) or intrinsic signals (mitochondrial stress), which then activate effector caspases (e.g., caspase-3, -6, -7) to degrade vital cellular components, ensuring orderly cell death with minimal inflammation[1][3][5]. Dysregulation of this pathway is central to many diseases, including cancer, neurodegeneration, inflammation, and transplantation injury, making the pathway and specific caspases attractive targets for drug development[4][6][2].
Caspase inhibition (blocks apoptosis) Activation of caspase cascade to induce cell death (anticancer) Modulation of regulatory proteins interacting with caspases (e.g., XIAP mimetics)
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