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There is a mounting body of evidence indicating a close association between cellular senescence and the underlying pathophysiology of AKI, as they both exhibit a cell cycle arrest at the G2/M phase, heightened oxidative stress, an increase in cyclin-dependent kinase inhibitors, telomere shortening, and an exacerbated in the fibrotic processes

doi: 10.1016/S1262-3636(08)73397-4 191 YeJ

Low GSH, neutrophil infiltration, myeloperoxidase activity and inflammation increase oxidative stress overwhelming the antioxidant defense, and hypochlorous acid mediated GSH oxidation and its attachment to proteins contribute to further GSH deficiency (114)

Large-scale, double-blind, placebo-controlled human randomized trials are lacking