Ovarian aging is increasingly recognized as a dynamic and modifiable process influenced by oxidative stress, mitochondrial dysfunction, and chronic inflammation. This review outlines the mechanisms by which environmental and lifestyle factors, such as smoking, high-fat diets, endocrine-disrupting chemicals, and micro- and nanoplastics (MNPs), contribute to accelerated ovarian decline and premature reproductive senescence. The distinction between physiological aging and pathological processes such as “inflamm-aging” is discussed, with particular attention to redox imbalance and mitochondrial impairment as key drivers of follicular depletion and endocrine dysfunction. Insights from experimental models of premature ovarian insufficiency and polycystic ovary syndrome are summarized to illustrate the role of reactive oxygen species and oxidative damage. Current antioxidant-based strategies aimed at delaying ovarian aging are reviewed, including melatonin, N-acetylcysteine, coenzyme Q10, polyphenols, and vitamins C and E. Particular emphasis is placed on the emerging potential of stem cell-derived extracellular vesicles (EVs) as a novel, cell-free therapeutic approach. Preclinical evidence suggests that EVs can reduce oxidative stress, support mitochondrial function, and restore ovarian physiology. Overall, the review highlights how redox-targeted and EV-based interventions may offer promising avenues to preserve ovarian function and extend reproductive healthspan.
Rapini et al. (2026) studied this question.