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In a cisplatin-induced POI rat model, exosomes enriched with miR-126-3p from UC-MSCs boosted ovarian angiogenesis, suppressed granulosa-cell apoptosis and normalised E, AMH and FSH levels by silencing PIK3R2 and engaging PI3K/AKT/mTOR signalling [21]

The literature supports preferential expression of fibroproliferative genes in patients with CCCA

These are likely downstream effects of improved mitochondrial and DNA function

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Metabolic disruption increases the risk of menstrual irregularity, ovulatory infertility, and adverse pregnancy outcomes