Cardiovascular Dysfunction in Polycystic Ovary Syndrome: Mitochondrial and Inflammatory Mechanisms

Polycystic ovary syndrome (PCOS) is a common endocrine disorder that significantly increases cardiovascular disease (CVD) risk in women. While insulin resistance and dyslipidemia are established contributors, growing evidence highlights mitochondrial dysfunction and chronic low-grade inflammation as central drivers of cardiovascular pathology in PCOS.

This narrative review synthesizes current evidence on how mitochondrial dysfunction and inflammation interact to promote cardiovascular complications in women with PCOS while identifying potential therapeutic targets and areas requiring further investigation.

A comprehensive review of clinical and experimental studies was conducted using PubMed, Scopus, and Web of Science databases. Relevant literature exploring mitochondrial alterations, oxidative stress, inflammatory cytokines, and endothelial function in PCOS, with emphasis on cardiovascular outcomes, was critically evaluated and summarized.

Women with PCOS exhibit altered mitochondrial dynamics, reduced ATP production, and elevated reactive oxygen species (ROS), which collectively impair vascular function. These mitochondrial abnormalities compromise oocyte quality and endometrial receptivity and activate proinflammatory signaling pathways, including the NLRP3 inflammasome, contributing to endothelial dysfunction and atherogenesis, and increased long-term cardiovascular risk, particularly in women with prior pregnancy complications. Elevated levels of cytokines including TNF-α, IL-6, and CRP further exacerbate cardiovascular risk. This bidirectional relationship between mitochondrial dysfunction and inflammation establishes a vicious cycle underlying cardiovascular deterioration in PCOS.

Mitochondrial dysfunction and inflammation are interdependent mechanisms that contribute substantially to cardiovascular risk in women with PCOS. Targeting mitochondrial dysfunction and systemic inflammation presents a promising therapeutic strategy for reducing cardiovascular morbidity in PCOS. Future research should emphasize phenotype-specific interventions, biomarker discovery, and translational trials to improve long-term reproductive and cardiovascular outcomes.