Mitochondrial apoptosis pathway core components (null)

The mitochondrial apoptosis pathway, also referred to as the intrinsic pathway of apoptosis, is a tightly regulated, cell-intrinsic mechanism of programmed cell death crucial for tissue homeostasis and response to cellular stress. Its core components include: - **Bcl-2 family proteins**: Regulate mitochondrial outer membrane permeabilization (MOMP); pro-apoptotic members (Bax, Bak) promote, anti-apoptotic (Bcl-2, Bcl-xL, Mcl-1) inhibit MOMP[1][2][4][5]. - **Cytochrome c**: Released from mitochondrial intermembrane space upon MOMP, activates cytosolic Apaf-1[1][2][5]. - **Apaf-1 (Apoptotic protease-activating factor 1)**: Oligomerizes with cytochrome c and dATP to form the apoptosome, which recruits and activates procaspase-9[1][4][5]. - **Caspase-9 and downstream effector caspases** (notably caspase-3): Initiate the proteolytic cascade that leads to cellular demolition[1][4][5]. - **Mitochondrial proteins Smac/DIABLO and Omi/HtrA2**: Released during MOMP, they inhibit inhibitor of apoptosis proteins (IAPs), further ensuring caspase activity[1][2][4][5]. - **Apoptosis-inducing factor (AIF) and endonuclease G**: Mediate caspase-independent pathways, leading to chromatin condensation and DNA fragmentation[1][5]. Dysregulation of these molecules plays a major role in disease, particularly in cancer (evasion of apoptosis), neurodegeneration (excessive apoptosis), and tissue injury. Many modern cancer therapeutics target components of this pathway, especially the Bcl-2 family[5]. Because "Mitochondrial pathway apoptosis components" is a plural and unspecific aggregate rather than a single standard drug target, it is not a conventional molecular entry, though the core pathway is among the most heavily investigated in apoptosis research and drug development[1][2][4][5].

Other names

intrinsic apoptosis pathway componentsmitochondrial-mediated apoptotic regulatorsintrinsic pathway of apoptosis

Induction or inhibition of mitochondrial outer membrane permeabilization (MOMP) (e.g., BH3 mimetics promote, Bcl-2 antagonists prevent); Caspase activation/inhibition; Modulation of inhibitor of apoptosis proteins (IAPs) via Smac mimetics; Induction of cytochrome c release