Mechanisms of Granulosa Cell Programmed Cell Death and Follicular Atresia in Polycystic Ovary Syndrome.

Abstract

Polycystic ovary syndrome (PCOS) is a common endocrine disorder affecting women of reproductive age, characterized by a spectrum of reproductive, endocrine, and metabolic disturbances. The etiology of PCOS encompasses a complex interplay of genetic, metabolic, inflammatory, and oxidative factors, though the precise pathological mechanisms remain inadequately understood. Despite considerable variability in the clinical characteristics and biochemical profiles among individuals with PCOS, abnormalities in follicular development are a hallmark of the condition. Granulosa cells, integral to follicular development, play a pivotal role in follicle maturation. Recent studies have established a strong correlation between granulosa cell programmed cell death and follicular atresia in PCOS. This review provides a comprehensive analysis of the current understanding of granulosa cell programmed cell death and its contribution to follicular atresia within the pathophysiology of PCOS, providing a foundation for future research endeavors. Key words Follicular atresia, Hyperandrogenism, Insulin resistance, Polycystic ovary syndrome, Programmed cell death of granulosa cells.