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On the other hand, the redox state disequilibrium or down modulation of GSH made these MDR cells more sensitive to chemotherapy [9]

E., Gishan, F

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targeted therapy in RCC)by clarifying disease-specific regulatory mechanisms: PKD1 mutation-driven mitochondrial defects in ADPKD, DPP9-Nrf2-mediated sorafenib resistance in RCC, and PPARFABP1 axis dysregulation in IgA nephropathy, alongside shared core pathways (e.g., GPX4/SLC7A11 as central checkpoints)

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