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Figure 4 Alterations in the intracellular redox status are often associated with GSH depletion (Polonikov, 2020) and endogenous GSH deficiency, due either to decreased biosynthesis and/or increased consumption, is a marked contributor to the pathogenesis of numerous diseases via mechanisms including oxidative stress and inflammation

In neonatal rat cardiomyocytes, mitochondrial p38 interacts with Mn Superoxide Dismutase, phosphorylating it at key residues, thereby reducing ROS and promoting survival, including in settings of 17-estradiolmediated protection [130, 138]

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