ArticleLife science alliance2024
VDR restores the expression of PINK1 and BNIP3 in TECs of streptozotocin-induced diabetic mice.
Article in Life science alliance, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed.
- Mitochondrial dysfunction-ferroptosis crosstalk drives renal fibrosis in chronic kidney disease.Renal failure · 2026Review
- Review
- Mitophagy in kidney and lung epithelial cells: molecular mechanisms, crosstalk, and therapeutic interventions.Frontiers in physiology · 2026Review
- Vitamin D receptor modulates autophagy via miR-20a-5p/ATG16L1 axis to alleviate lipopolysaccharide-induced acute kidney injury.Renal failure · 2025Article
- miR-17-5p Inhibits BNIP3-Mediated Mitochondrial Autophagy to Attenuate Pathological Cardiac FibrosisBalkan medical journal · 2025Article
- Protective role of vitamin D receptor against mitochondrial calcium overload from PMRedox biology · 2025Article
- Vitamin D and chronic kidney disease: mechanisms, clinical implications, and future perspectives.Frontiers in medicine · 2025Review
- Pharmacological potential of Chinese botanical drugs in managing chronic kidney disease by targeting mitochondrial quality control.Frontiers in pharmacology · 2025Review
- Altered mitochondrial function: a clue therapeutic strategies between metabolic dysfunction-associated steatotic liver disease and chronic kidney disease?Frontiers in nutrition · 2025Review
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Authors and funding
11 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Defective mitophagy in renal tubular epithelial cells is one of the main drivers of renal fibrosis in diabetic kidney disease. Our gene sequencing data showed the expression of PINK1 and BNIP3, two key molecules of mitophagy, was decreased in renal tissues of VDR-knockout mice. Herein, streptozotocin (STZ) was used to induce renal interstitial fibrosis in mice. VDR deficiency exacerbated STZ-induced renal impairment and defective mitophagy. Paricalcitol (pari, a VDR agonist) and the tubular epithelial cell-specific overexpression of VDR restored the expression of PINK1 and BNIP3 in the renal cortex and attenuated STZ-induced kidney fibrosis and mitochondrial dysfunction. In HK-2 cells under high glucose conditions, an increased level of α-SMA, COL1, and FN and a decreased expression of PINK1 and BNIP3 with severe mitochondrial damage were observed, and these alterations could be largely reversed by pari treatment. ChIP-qPCR and luciferase reporter assays showed VDR could positively regulate the transcription of
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