Recent advances in inflammation & allergy drug discovery · 2026
Inflammation-Driven Pathogenesis of Polycystic Ovary Syndrome: Integrating Endocrine Imbalance, Reproductive Impairments, and Tissue-Level Change.
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Suthar Manthan, Kaliberdenko Vitalii
Аннотация
BACKGROUND: Polycystic ovary syndrome (PCOS) is a common endocrine disorder in women of reproductive age, classically defined by hyperandrogenism, ovulatory dysfunction and polycystic ovaries morphology. Recent findings now support that low-grade chronic inflammation is a key player in PCOS pathophysiology, explaining hormonal, metabolic, and reproductive dysfunction.
OBJECTIVE: The objective of this narrative review is to update the readership regarding the role of inflammation as a driver in the pathogenesis of PCOS, particularly at points where inflammatory and endocrine, reproductive, and tissue levels intersect.
METHOD: We performed a narrative review using published, peer-reviewed, and library-recorded sources available in databases such as PubMed, Scopus, and Web of Science. Keywords relevant to PCOS, fibrosis, endocrine dysfunction, inflammation and reproductive impairment were employed. studies were chosen to be included in this review based on their relevance, quality and concentration on inflammatory pathways and tissue-level changes in PCOS. Results were synthesised thematically in order to synthesize understanding mechanisms between the molecular, endocrine and clinical levels.
RESULTS: There is evidence that insulin resistance, hyperandrogenism, and dysfunction of the hypothalamic-pituitary-ovarian axis are associated with pro-inflammatory cytokines and immune dysregulation and oxidative stress. Inflammatory signaling also plays a role in follicular development, ovarian tissue remodeling and adipose tissue function. These elements of an feed-forward loop maintain the endocrine and metabolic features of Conclusion: Inflammation seems to be a primary determinant in the pathogenicity of PCOS and not mere secondary phenomenon. The identification of the development of inflammation opens the possibility of novel treatment paradigms including anti-inflammatory treatments such as those used for PCOS patients presenting with reproductive and metabolic abnormalities.
OBJECTIVE: The objective of this narrative review is to update the readership regarding the role of inflammation as a driver in the pathogenesis of PCOS, particularly at points where inflammatory and endocrine, reproductive, and tissue levels intersect.
METHOD: We performed a narrative review using published, peer-reviewed, and library-recorded sources available in databases such as PubMed, Scopus, and Web of Science. Keywords relevant to PCOS, fibrosis, endocrine dysfunction, inflammation and reproductive impairment were employed. studies were chosen to be included in this review based on their relevance, quality and concentration on inflammatory pathways and tissue-level changes in PCOS. Results were synthesised thematically in order to synthesize understanding mechanisms between the molecular, endocrine and clinical levels.
RESULTS: There is evidence that insulin resistance, hyperandrogenism, and dysfunction of the hypothalamic-pituitary-ovarian axis are associated with pro-inflammatory cytokines and immune dysregulation and oxidative stress. Inflammatory signaling also plays a role in follicular development, ovarian tissue remodeling and adipose tissue function. These elements of an feed-forward loop maintain the endocrine and metabolic features of Conclusion: Inflammation seems to be a primary determinant in the pathogenicity of PCOS and not mere secondary phenomenon. The identification of the development of inflammation opens the possibility of novel treatment paradigms including anti-inflammatory treatments such as those used for PCOS patients presenting with reproductive and metabolic abnormalities.