Polycystic ovary syndrome (PCOS) is a multifactorial endocrine disorder characterized by hyperandrogenism, inflammation, and ovarian dysfunction. While exercise has been recognized as an effective non-pharmacological strategy for managing PCOS symptoms, the molecular mechanisms underlying its therapeutic benefits remain unclear. In this study, we utilized a dehydroepiandrosterone-induced PCOS mouse model to investigate how aerobic exercise ameliorates ovarian pathology. Our results demonstrated that exercise restored the estrous cycle, reduced ovarian cyst formation, and alleviated ovarian fibrosis and inflammation. Exercise upregulated ATP-dependent protease Lon peptidase 1 (LONP1) expression, accompanied by normalization of key steroidogenic protein levels, cytochrome P450 side-chain cleavage enzyme (CYP11A1) and steroidogenic acute regulatory protein (StAR). In parallel, exercise activated AMP-activated protein kinase (AMPK), which was accompanied by restoration of LONP1-associated mitochondrial proteolytic capacity and normalization of steroidogenic enzyme turnover. Exercise also enhanced mitochondrial biogenesis related markers, including peroxisome proliferator-activated receptor gamma coactivator 1-alpha (PGC-1α) and peroxisome proliferator-activated receptor-alpha (PPARα), suggesting improved mitochondrial homeostasis in the PCOS ovary.
Shin et al. (2026) studied this question.