Feed

Polycystic ovary syndrome (PCOS) is a heterogeneous endocrine-metabolic disorder characterized by dysregulated ovarian signaling, metabolic inflammation, insulin resistance, and aberrant angiogenesis, for which effective disease-modifying therapies remain limited. Resveratrol (RES), a pleiotropic polyphenol, has attracted increasing attention for its ability to modulate multiple molecular and cellular pathways implicated in PCOS pathophysiology. In this review, we synthesize current evidence to clarify how RES regulates key pathological signaling networks in PCOS, including ovarian follicular dysfunction, impaired insulin signaling, hyperandrogenism, oxidative stress, and vascular remodeling. Rather than merely cataloguing isolated mechanisms, we integrate findings from experimental models to highlight major convergent nodes-such as phosphoinositide 3-kinase (PI3K)/protein kinase B (Akt)/mechanistic target of rapamycin (mTOR), sirtuin 1 (SIRT1)/AMP-activated protein kinase (AMPK), nuclear factor kappa-B (NF-κB), and vascular endothelial growth factor (VEGF)-related pathways-through which RES may exert coordinated regulatory effects at the cellular and tissue levels. We further examine the available clinical studies to assess the translational relevance of these mechanistic insights, with particular emphasis on phenotypic heterogeneity, dose dependence, and the treatment window. Although clinical outcomes remain modest and variable, the available evidence suggests that RES may provide context-dependent benefits in selected PCOS subtypes. Collectively, this review offers a network-based framework linking the molecular actions of RES to the complex pathophysiology of PCOS and identifies key knowledge gaps that must be addressed to improve translational precision and therapeutic applicability.