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Description
In the pathogenesis of cardiovascular diseases, excessive ROS production disrupts mitochondrial function, amplifies inflammatory responses, and induces significant cellular damage, such as myocardial fibrosis, cardiomyocyte apoptosis, and extracellular matrix degradation [127, 128]

As the embryo enters the uterus, endometrial epithelial-derived EVs (EE-EVs) contribute to endometrial receptivity

In this model, lipid changes typical of ferroptosis, as well as induction of the ferroptosis marker TfR1 were reported (Bednash et al., 2021)

Loeppky C, Tarka E
