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Clinical studies and preclinical models suggest that Tim-3-expressing macrophages, whose renal expression correlates with the severity of diabetic nephropathy, induce podocyte injury through the NF-B/Tumor necrosis factor-alpha (TNF-) pathway, with reduced nephrin expression being inversely associated with macrophage activation (34)

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This loss of GSH occurs through several mechanisms, including direct enzymatic GSH oxidation to GSSG by GPX4 during reduction of hydroperoxy-phospholipids, export of GSSG, and dependence on the continuous availability of newly formed GSH

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