Granulosa Cell Autophagy in Pathophysiological Mechanism of Polycystic Ovary Syndrome

doi:10.12280/gjszjk.20230483

Abstract

Abstract:

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.

Key words: Polycystic ovary syndrome, Ovarian follicle, Autophagy, Autophagy-related proteins, Granulosa cell

ZHEN Jia, ZHAO Zi-yuan, WANG Zi-lu, SHI Wei, XU Li. Granulosa Cell Autophagy in Pathophysiological Mechanism of Polycystic Ovary Syndrome[J]. Journal of International Reproductive Health/Family Planning, 2024, 43(2): 150-154.

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