Women with PCOS (n=43) displayed impaired autophagy and mitophagy in immune cells, elevated oxidative stress, and increased neutrophil-endothelial interactions compared to controls (n=48).
Cross-Sectional (n=91)
Are autophagy and mitophagy impaired in circulating immune cells of women with PCOS compared to controls?
Impaired autophagy and mitophagy in immune cells of women with PCOS are linked to oxidative stress, inflammation, and early endothelial dysfunction, highlighting a potential mechanism for their increased cardiometabolic risk.
Polycystic ovary syndrome (PCOS) is a complex endocrine disorder associated with systemic inflammation, oxidative stress, and increased cardiometabolic risk. While impaired autophagy and mitophagy have been implicated in tissue-specific dysfunction, their role in circulating immune cells and relation to early vascular alterations remain unclear. In this cross-sectional study, 91 women (48 controls, 43 with PCOS) underwent anthropometric and biochemical assessment. Systemic markers included myeloperoxidase (MPO), glutathione, TNFα, and sP-selectin were determined in serum. Superoxide production (dHE), mitochondrial membrane potential (TMRM), and protein levels of BECLIN1, LC3II/I, P62, NBR1, and PINK1 were assessed in peripheral blood mononuclear cells (PBMCs). Neutrophil-endothelial cell interactions were analysed as subclinical markers of endothelial dysfunction. PCOS patients presented hormonal, lipid, and glucose abnormalities, accompanied by redox imbalance, elevated MPO and superoxide levels, reduced glutathione, and increased mitochondrial membrane potential. Autophagy and mitophagy pathways were significantly impaired in PBMCs, and the expression of all assessed markers was reduced. These alterations were associated with androgen excess, oxidative stress, and inflammation. Elevated sP-selectin and enhanced neutrophil-endothelial interactions indicated early endothelial dysfunction in PCOS women. Our findings reveal that women with PCOS display autophagy and mitophagy impairment in immune cells, processes that are linked to oxidative and inflammatory stress and accompanied by endothelial alterations, highlighting a potential mechanistic pathway contributing to their cardiometabolic risk. • Autophagy and mitophagy proteins are downregulated in PBMCs from PCOS patients. • Oxidative stress markers are elevated systemically and in immune cells in PCOS. • Autophagy dysregulation is linked to hormonal imbalance and systemic inflammation. • PCOS women show increased neutrophil-endothelial interactions and sP-selectin. • Mitochondrial dysfunction and redox imbalance coexist in PBMCs from PCOS women.
Pelechá-Salvador et al. (Sun,) conducted a cross-sectional in Polycystic ovary syndrome (PCOS) (n=91). Polycystic ovary syndrome vs. Healthy controls was evaluated on Autophagy and mitophagy markers in PBMCs, systemic oxidative stress, and neutrophil-endothelial cell interactions. Women with PCOS (n=43) displayed impaired autophagy and mitophagy in immune cells, elevated oxidative stress, and increased neutrophil-endothelial interactions compared to controls (n=48).