Mitochondrial apoptosis

Mitochondrial apoptosis (the intrinsic pathway of apoptosis) is a tightly regulated process of programmed cell death, initiated by intracellular stress signals (such as DNA damage) that trigger a series of molecular events in mitochondria[1][3][5]. Central to this process are members of the Bcl-2 family, which tightly control mitochondrial outer membrane permeabilization (MOMP). Upon activation, pro-apoptotic proteins (Bax, Bak) form pores in the mitochondrial outer membrane, enabling the release of cytochrome c and other pro-apoptotic factors (e.g., SMAC, Apaf-1) into the cytosol. This cascade results in the activation of caspases, ultimately leading to cellular disassembly and efficient clearance by phagocytes. Dysregulation of mitochondrial apoptosis has major implications in diseases such as cancer, neurodegeneration, and ischemic injury[5][2][3]. Therapeutic approaches aim to either induce mitochondrial apoptosis (in cancer) or prevent it (in neurodegeneration, ischemic injury) by targeting specific molecules within the pathway—not the overall process itself[2][4][6].

Other names

Intrinsic apoptosis pathwayMitochondria-mediated apoptosisMitochondrial pathway of apoptosis

Induction of mitochondrial outer membrane permeabilization (MOMP) via Bcl-2 family modulation Release of cytochrome c and other apoptogenic factors Activation of caspases ROS generation and modulation of mitochondrial metabolism[1][4][5]