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Another research examined the cardioprotective mechanisms exerted by EGT within an experimental rat model of MI

Vega-Naredo, I

In contrast, excessive or unregulated ROS production can compromise mitochondrial membrane potential, trigger cytochrome c (Cyt c) release, and induce oocyte apoptosis through the Bax/Bak-dependent mitochondrial apoptotic pathway, potentially leading to follicular atresia or depletion of the ovarian reserve [34, 35]