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In cases of diabetic nephropathy, chronic hyperglycemia induces the formation of autoantibodies against podocyte antigens, which cross-react with glomerular components, triggering complement activation and foot process effacement

This exposure results in the creation of aqueous pores within the lamellar lipid regions of the SC, thereby facilitating the drug diffusion across the skin barrier [192, 244]
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Carboxy-PTIO (cPTIO), a known NO scavenger [31], was used to probe the role of cellular NO in erastin-induced cell death
