多囊卵巢综合征病理机制中的颗粒细胞自噬

Granulosa Cell Autophagy in Pathophysiological Mechanism of Polycystic Ovary Syndrome

多囊卵巢综合征(polycystic ovary syndrome,PCOS)是育龄期女性最常见的生殖内分泌紊乱性疾病之一,病理机制尚未阐明。自噬参与卵泡发育的各个阶段,其中卵泡颗粒细胞自噬相对活跃。通过维持颗粒细胞自噬的稳态支持卵巢功能、调控卵泡发育,最终影响胚胎质量及妊娠结局。自噬相关基因和蛋白的异常表达可激活不同的自噬通路,抑制卵泡颗粒细胞发育、干扰内分泌稳态,参与PCOS的病理过程,并影响其预后。综述参与颗粒细胞自噬的关键分子及其在PCOS发生发展中的作用,以期为研究PCOS发生机制及探索临床治疗提供参考。

Polycystic ovary syndrome(PCOS)is one of the most common reproductive endocrine disorders in women of reproductive age,and the pathophysiological mechanisms have not been elucidated.Autophagy participates in the all stages of follicular development,in which autophagy is relatively high-activated in the follicular granulosa cells.To maintain the autophagy homeostasis will support ovarian function and regulate follicular development,and ultimately affect the embryo quality and pregnancy outcomes.Abnormal expressions of autophagy-related genes and proteins can activate different pathways of autophagy,inhibit follicular granulosa cell development and interfere with endocrine homeostasis,which participates in the pathological process and prognosis of PCOS.This paper reviews the research progress of key molecules involved in granulosa cell autophagy in endocrine metabolism and the pathological roles of autophagy in PCOS,which provides more references for us to explore the mechanism of PCOS and clinical treatment.