Gut microbiota and polycystic ovary syndrome: Pathogenesis and novel therapeutic approaches

Polycystic ovary syndrome (PCOS) is a common endocrine and metabolic disorder in women that is characterized by a complex pathogenesis involving multiple mechanisms, including hyperandrogenism, ovulatory dysfunction, insulin resistance (IR), and chronic inflammation. Recent studies have demonstrated that the gut microbiota acts as an important metabolic regulator and may play a pivotal role in the onset and progression of PCOS. Patients with PCOS frequently exhibit gut microbiota dysbiosis, which is characterized by reduced microbial diversity, decreased levels of beneficial bacteria, increased levels of pathogenic bacteria, and altered metabolic byproducts. This imbalance may contribute to IR and ovarian dysfunction by activating the toll-like receptor 4/nuclear factor kappa B inflammatory pathway, inducing oxidative stress, and disrupting Wnt/β-catenin signaling. The Wnt/β-catenin signaling pathway, a key regulator of follicular development, is frequently aberrantly activated in PCOS. In this narrative review, we summarize the recent advances in understanding the roles of the gut microbiota and the Wnt/β-catenin signaling pathway in the pathogenesis of PCOS. To this end, we conducted a comprehensive literature search across PubMed, Web of Science, Embase, and Cochrane Library databases, covering publications from January 2012 to March 2026. Ninety-eight articles were included after screening. We further explored therapeutic strategies based on microbiome modulation and signaling pathway targeting, including probiotics, traditional Chinese medicine, ginsenosides, puerarin, fecal microbiota transplantation, and nanoparticle-based ginseng-derived exosomes, thereby providing novel insights into potential therapies for PCOS.