Insulin resistance, inflammation, oxidative stress and dysregulated WNT/β-Catenin signaling in polycystic ovary syndrome: A review.

Polycystic ovary syndrome (PCOS) is a multifaceted reproductive and endocrine health issue affecting reproductive aged women, characterized by insulin resistance (IR), chronic low-grade inflammation (LGI), oxidative stress (OS) and dysregulated WNT/β-catenin signaling pathway. Although a part of the involved mechanism in PCOS occurrence is discovered, the exact etiology involving intricate relationships between OS, inflammatory markers and dysregulated WNT/β-catenin signaling pathway in PCOS are still unknown. This review aimed to explore the interplay between IR, LGI, OS and dysregulated WNT/β-catenin signaling pathway in the pathophysiology of PCOS. A comprehensive literature search was conducted to identify relevant studies investigating the role of OS, inflammatory markers and WNT/β-catenin signaling in PCOS. Databases including PubMed, Scopus, Web of Science and Google Scholar were searched using keywords as, "PCOS and oxidative stress", "Insulin Resistance and PCOS", "Inflammation and PCOS", "WNT/β-catenin signaling in PCOS". The search was limited to studies published in English up to 2025 without any restrictions on publication year. In conclusion, PCOS is a complex and multifactorial disorder driven by the intricate involvement of insulin resistance, chronic low-grade inflammation, oxidative stress and dysregulated WNT/β-catenin signaling pathway among reproductive age women. Although substantial progress has been made in elucidating these interconnected mechanisms, the etiological pathways remain incompletely understood. The evidences collected in this study highlights that these physiological and signaling factors do not act in isolation but collectively contribute to the initiation and progression of various pathological mechanisms of PCOS among young women. A deeper understanding of their physiological and molecular crosstalk is essential for identifying reliable biomarkers and novel therapeutic targets.