Mechanisms and clinical implications of oxidative stress-mediated endometrial receptivity impairment in polycystic ovary syndrome

Polycystic ovary syndrome (PCOS) is a common reproductive and metabolic disorder with a complex and yet unresolved etiology. Although ovulation induction therapy can improve ovulatory function, the natural pregnancy rate and pregnancy outcomes in women with PCOS remain suboptimal, suggesting that impaired Endometrial receptivity (ER) may represent a key pathological link. Accumulating evidence suggests that Oxidative stress (OS) is closely associated with impaired ER, as excessive ROS impair endometrial function through mitochondrial damage and activation of inflammatory pathways. This review systematically evaluates the direct and indirect evidence concerning the role of the gut and endometrial microbiota in PCOS-related endometrial dysfunction, and explores its potential mechanisms in influencing ER via OS pathways. We integrate how Insulin resistance (IR), hyperandrogenism, and microbial dysbiosis collectively drive the endometrial oxidative-inflammatory network. proposing a Microbiota-first hierarchical framework to conceptualize potential pathological links underlying infertility in PCOS.