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Paricasitol as a VDR agonist can inhibit ferroptosis by activating VDR/Nrf2/HO1 signaling pathway in DN, which effectively attenuates iron deposition in renal tubular epithelial cells and renal damage after diabetic injury [82]

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Increased PTMs of mitochondrial proteins inactivate many enzymes involved in the reduction of oxidative species, fatty acid metabolism, and mitophagy pathways, leading to mitochondrial dysfunction, energy depletion, and apoptosis