VDR-KO exacerbated the impairment of mitophagy with promoted renal impairment and fibrosis in diabetic mice, whereas VDR activation with the agonist paricalcitol or TEC-specific VDR overexpression markedly restored the expression of BNIP3 and PINK1, attenuated mitochondrial morphology, and alleviated renal fibrosis. This evidence concerns the gene BNIP3 and renal fibrosis.