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The results showed that VRK2 knockdown could induce an increase of ROS and decline of cell viability and GSH following TBHP treatment, while these alterations could be partly reversed by ectopic SLC7A11 expression but not GCLC or GSS expression (Fig

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These metabolic changes lead to glomerular hyperfiltration, enlargement, and increased proximal tubular glucose reabsorption via sodium-glucose cotransporter 2, resulting in elevated intraglomerular pressure and hyperfiltration [25]