Follicular granulosa cell apoptosis

Follicular granulosa cell apoptosis is a fundamental biological process characterized by the programmed cell death of granulosa cells within the ovarian follicle, primarily serving as the mechanism for follicular atresia [4, 11]. This process is tightly regulated by a balance of survival factors, such as follicle-stimulating hormone (FSH) and estrogen, and pro-apoptotic signals, including Caspase-3, BAX, and FoxO1 [6, 11, 13]. In a healthy ovary, more than 99% of follicles undergo atresia via this apoptotic pathway, ensuring that only a dominant follicle reaches ovulation in each cycle [12, 18]. Dysregulation of this process is a hallmark of major reproductive disorders: excessive apoptosis is a primary cause of premature ovarian failure (POF) and reproductive aging, while abnormally low levels of apoptosis contribute to the characteristic accumulation of small antral follicles in polycystic ovary syndrome (PCOS) [1, 6, 14]. Therapeutic interventions often target this pathway by utilizing gonadotropins (e.g., recombinant FSH) to promote survival signaling through the PI3K/Akt/mTOR pathway or by using antioxidants like resveratrol and vitamin E to mitigate oxidative stress-induced cell death [1, 10, 16]. Understanding and modulating granulosa cell apoptosis is therefore critical for managing infertility, enhancing the success of assisted reproductive technologies, and preserving ovarian function [2, 12, 13].

Other names

Granulosa cell apoptosisOvarian follicular atresiaGranulosa cell programmed cell deathGC apoptosis

Modulation of the intrinsic and extrinsic apoptotic pathways via activation of survival signaling (PI3K/Akt/mTOR), inhibition of executioner caspases (Caspase-3), and transcriptional regulation of BCL-2 family proteins and FoxO1.