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Ovarian granulosa cell apoptosis is the process by which granulosa cells within the ovarian follicle undergo programmed cell death, a key event governing follicular atresia (degeneration of non-dominant follicles), and ultimately, the regulation of female fertility and reproductive lifespan. Granulosa cell apoptosis is triggered by both intrinsic (mitochondrial) and extrinsic (death receptor-mediated) pathways, involving regulatory molecules such as Bcl-2 family proteins, caspases, the Fas/FasL system, and is affected by oxidative stress and hormonal signals. This process is a primary determinant of follicle pool size and is implicated in conditions including premature ovarian insufficiency and age-related reproductive decline. Although not itself a “target,” the molecular regulators of granulosa cell apoptosis (e.g., Bcl-2, Fas receptor, TGFBR2, miRNAs such as miR-187, lncRNA NORHA) may be therapeutic targets for interventions aiming to preserve follicle number or treat female infertility. Note: "Ovarian granulosa cell apoptosis" is a cellular process, not a discrete molecular target or receptor. For drug development or mechanistic studies, focus shifts to individual apoptosis-regulating molecules (such as Bcl-2, Fas receptor, TGF-β, MAPK, PI3K-Akt) or signaling pathways (e.g., TGF-β, MAPK, PI3K-Akt), not the phenomenon as a whole.
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