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Polycystic ovary syndrome (PCOS) is a prevalent endocrine disorder and a leading cause of infertility primarily due to impaired folliculogenesis and anovulation. Central to ovarian function and follicular development is the extracellular matrix (ECM), which undergoes significant remodeling facilitated by matrix metalloproteinases (MMPs). In PCOS, the ovarian cortex becomes thickened and collagen-rich, creating a rigid environment that disrupts normal follicular growth and oocyte maturation. Altered MMP activity further complicates this scenario by impairing ECM degradation, leading to the accumulation of small, quiescent follicles, and elevated androgen levels. This review aims to explore the intricate roles of ECM and MMP alterations in PCOS pathogenesis, highlighting their impact on folliculogenesis and steroidogenesis. Understanding MMP/TIMP dynamics offers insights into potential therapeutic targets to restore normal ovarian function and improve fertility outcomes for women with PCOS.
Nikanfar et al. (Thu,) studied this question.