Caspase-mediated apoptosis pathway activation

The **caspase-mediated apoptosis pathway** is a well-characterized process wherein the activation of caspases (cysteinyl aspartate-specific proteases) leads to the execution of programmed cell death, or apoptosis. There are two principal activation arms: the extrinsic (death receptor) pathway and the intrinsic (mitochondrial) pathway. In the extrinsic pathway, ligation of death receptors such as Fas or tumor necrosis factor receptor (TNFR) recruits adaptor proteins (e.g., FADD) that activate initiator caspases such as caspase-8. The intrinsic pathway involves mitochondrial outer membrane permeabilization, release of cytochrome c, apoptosome formation (Apaf-1 and pro-caspase-9), and subsequent activation of effector caspases (caspase-3, -7)[1][2][3][4][5]. Activated caspases cleave substrates resulting in the biochemical and morphological features of apoptosis. Aberrations in caspase-mediated apoptosis are involved in diseases including cancer, inflammatory and degenerative disorders, and therapeutic strategies often aim to modulate this pathway for clinical benefit[3][5]. **Note:** This query describes a biological process rather than a specific molecular drug target. For database and structured data use, it is important to instead refer to the individual caspase family members (such as "Caspase-3", "Caspase-8", "Caspase-9") which are canonical molecular targets within this pathway.

Other names

Caspase pathway activationCaspase-dependent apoptosisCaspase-mediated cell deathCaspase activation pathway

Inhibition of caspase activity (caspase inhibitors)[2] Induction of caspase-dependent apoptosis (death receptor agonists, chemotherapeutics)[3] Blockade or restoration of extrinsic/intrinsic apoptosis triggers