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Accumulating evidence indicates that AKI is not merely a transient hemodynamic disturbance but a biologically orchestrated process in which dysregulated intracellular signaling pathways translate ischemic stress into sustained renal injury and long-term functional decline

Depletion of intracellular GSH in HepG2 cells with BSO treatment was without effect on cell viability as assessed by MTT assay (Fig

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After the final heat-shock at 65 C the samples were centrifuged at 20,000 g and 4 C for 10 min

This review consolidates recent findings indicating that FOXO4-dependent senescence significantly contributes to neuroinflammation, synaptic dysfunction, and impaired neurogenesis in the aging brain