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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

We use clinical photography (front, three-quarter, profile, under cross-polarized light) to document the baseline, the four-week milestone, and the three-month outcome so progress is measurable rather than felt

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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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