<p>Polyendocrine metabolic ovarian syndrome (PMOS) remains a leading cause of anovulatory infertility worldwide, traditionally managed through systemic hormonal and metabolic stabilization. However, recent evidence has increasingly identified ovarian fibrosis, which is characterized by excessive extracellular matrix deposition and structural remodeling, as a critical hallmark of reproductive decline in affected individuals. This review provides a comprehensive synthesis of the evolving PMOS landscape, bridging the gap between classic endocrine dysfunction and the newly recognized fibrotic microenvironment. We systematically evaluate the pathogenesis of PMOS, ranging from hyperandrogenemia and insulin resistance to chronic low-grade inflammation, while detailing the molecular drivers of fibrosis such as the TGF-β/CTGF axis and mitochondrial exhaustion. Furthermore, we analyze current therapeutic modalities, including pharmacological agents, regenerative medicine, and traditional Chinese medicine, which highlight a paradigm shift toward precision interventions. Despite these advancements, the precise causal mechanisms linking PMOS to fibrotic pathology remain underexplored, and targeted curative strategies are scarce. We conclude by proposing that alleviating ovarian fibrosis through drug, metabolic, and immunomodulatory pathways represents a high-potential frontier. Future research should prioritize these anti-fibrotic strategies to not only alleviate symptoms but also fundamentally restore ovarian function and extend reproductive longevity.</p>