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Defective placentation leads to placental hypoxia and reperfusion injury due to ischemia and the resultant OS triggers the release of cytokines and prostaglandins, which results in endothelial cell dysfunction and plays an important role in the development of pre-eclampsia [77, 78]

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In the PCOS rat model induced by dehydroepiandrosterone, EVs from adipose derived mesenchymal stem cells (AMSC) and their derived EVs can be partially mediated by miR-21-5P, regulating liver glucose homeostasis by targeting B cell translocation gene 2 (BTG2), significantly alleviating multiple phenotypes of PCOS rats, including metabolic abnormalities, polycystic ovaries, and infertility ( 3.1.4 EVs regulate sugar and lipid metabolism and affect obesity Obesity promotes the development of PCOS, which in turn exacerbates obesity (Teede et al., 2023)

Variable selected post-translational modifications were carbamidomethyl (C), oxidation (M), deamidation (NQ), and phosphorylation (STY)