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The mitochondria-mediated apoptosis pathway, also known as the intrinsic apoptosis pathway, is a central mechanism by which cells undergo programmed cell death in response to internal stress signals. This pathway is tightly regulated and involves a cascade of molecular events that lead to the controlled dismantling and removal of damaged or unwanted cells. The balance between pro-survival and pro-apoptotic Bcl-2 family members determines cell fate under stress conditions; dysregulation can contribute to diseases like cancer or neurodegeneration. The pathway is activated by various intracellular stresses such as DNA damage, oncogene activation, hypoxia, deprivation of growth factors, or exposure to chemotherapeutic agents. Key steps include mitochondrial outer membrane permeabilization (MOMP), release of intermembrane space proteins (e.g., cytochrome c, SMAC/DIABLO), apoptosome formation, and caspase cascade activation.
Various, depending on the specific drug and its target within the pathway (e.g., BH3 mimetics inhibit pro-survival Bcl-2 family members)
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