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The mitochondrial pathway of apoptosis induction, also known as the intrinsic apoptotic pathway, is a cellular signaling cascade that leads to programmed cell death in response to internal stress signals such as DNA damage, oxidative stress, or hypoxia. This process is regulated by members of the Bcl‑2 protein family. Pro-apoptotic factors like Bax and Bak promote mitochondrial outer membrane permeabilization (MOMP), resulting in the release of cytochrome c and other pro-apoptotic factors from the intermembrane space into the cytosol. Cytochrome c then binds Apaf‑1 to form an apoptosome complex that activates initiator caspase‑9, which subsequently triggers executioner caspases such as caspase‑3 leading to cellular demolition. Anti-apoptotic Bcl‑2 family members inhibit this process by stabilizing mitochondrial membranes[1][4][5]. The mitochondrial apoptosis machinery plays a central role in cancer biology and therapy resistance; several anticancer agents act by modulating components within this pathway[1]. **Important note:** "Mitochondrial pathway of apoptosis induction" refers to a biological process or signaling cascade—not a single molecular target such as a receptor or enzyme. Therefore, it is not considered a therapeutic target per se but rather describes an entire mechanism involving multiple molecular targets including Bcl‑2 family proteins, cytochrome c, Apaf‑1, and various caspases[4][5].
Induction of mitochondrial outer membrane permeabilization (MOMP) via Bcl‑2 family modulation; Release of cytochrome c and activation of caspase cascade
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