ArticleDiabetes, metabolic syndrome and obesity : targets and therapy2024
MicroRNA-204-5p Ameliorates Renal Injury via Regulating Keap1/Nrf2 Pathway in Diabetic Kidney Disease.
Article in Diabetes, metabolic syndrome and obesity : targets and therapy, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 13 citations in OpenAlex.
- Integrated Analysis of Rat Pulmonary Hypertension Datasets Identifies Candidate circRNA Networks in Hypoxia-Exposed Pulmonary Artery Tissue.International journal of molecular sciences · 2026Article
- Suppressive effect of chrysin on macrophage LC3B autophagy through miR-204-5p in diabetic atherosclerosis.Scientific reports · 2026Article
- Urinary MicroRNA Expression and Tacrolimus Pharmacokinetic Variability in Kidney Transplant Recipients: A Cross-sectional Study.Clinical drug investigation · 2026Article
- MicroRNA Regulation in Kidney Interstitial Fibrosis.Epigenomes · 2026Review
- Endothelial progenitor cell derived extracellular vesicles promotes wound healing in diabetic mice via activating mobilization and neovascularization.Cell biology and toxicology · 2026Article
- Buspirone attenuates cyclophosphamide-induced renal dysfunction in association with alterations in miR-205/EGLN2, Nrf2, and PERK/ATF4/CHOP signaling.Frontiers in pharmacology · 2026Article
- Type IV Collagen-Targeting Nanoparticles for Efficient Delivery to the Renal Interstitium in Fibrotic Kidneys.Current drug delivery · 2026Article
- Trans-Coumaryl acetate mediates GRK5/NF-κB/Nrf2 signaling axis to ameliorate septic acute kidney injury.Journal of cell communication and signaling · 2025Article
- RGS12 is a target of penehyclidine hydrochloride that enhances oxidative stress and ferroptosis in a model of myocardial ischemia/reperfusion injury by inhibiting the Nrf2 pathway.International journal of molecular medicine · 2025Article
- Mechanism of action and potential therapeutic targets of TGF-β-related signaling pathway and its downstream miRNA expression in pulmonary arterial hypertension.Frontiers in pharmacology · 2025Review
- Programmed Cell Death in Diabetic Kidney Disease: Mechanisms and Therapeutic Targeting.Journal of inflammation research · 2025Review
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Authors and funding
9 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: Diabetic kidney disease (DKD) is characterized by renal fibrosis, and the pathogenesis of renal fibrosis is still not definitely confirmed. MiR-204-5p plays an important role in the regulation of fibrosis, autophagy and oxidative stress. In this study, we aimed to investigate the role of miR-204-5p on renal damage in diabetic kidneys and the underlying mechanisms involved. Methods: In vivo, AAV-Ksp-miR-204-5p mimics were injected into mice via tail vein. In vitro, high glucose-induced HK-2 cells were treated with miR-204-5p inhibitor, miR-204-5p mimics, ATG5 siRNA, tertiary butyl hydroquinone (TBHQ), ML385, or 3-Methyladenine (3-MA). FISH and qRT-PCR were used to detect miR-204-5p expression. The expressions of protein and mRNA were detected by Western blotting, immunofluorescence, immunohistochemistry and qRT-PCR. The concentration of fibronectin in HK-2 cells culture medium was detected by ELISA. Results: The expression of miR-204-5p in diabetic kidneys was significantly inhibited than that in control group. Delivering miR-204-5p mimics increased miR-204-5p expression, improved renal function, inhibited renal fibrosis and oxidative stress, and restored autophagy in db/db mice. In vitro, the expression of miR-204-5p was inhibited by HG treatment in HK-2 cells. MiR-204-5p mimics effectively increased miR-204-5p expression and reduced fibronectin and collagen I expression, restored autophagy dysfunction, and increased Nrf2 expression, whereas these alterations were abrogated by Nrf2 inhibitor ML385, autophagy inhibitor 3-methyladenine (3-MA, 5 mM) treatment or ATG5 siRNA transfection in HG-induced HK-2 cells. In addition, miR-204-5p inhibitor significantly inhibited miR-204-5p expression and aggravated HG-induced fibronectin and collagen I expression, autophagy dysfunction, and decreased Nrf2 expression, while these alterations were abolished by Nrf2 activator TBHQ. Furthermore, the binding of miR-204-5p with Keap1 was confirmed by luciferase reporter assay and miR-204-5p negatively regulated Keap1 expression, resulting in the activation of Nrf2 pathway. Conclusion: MicroRNA-204-5p protects against the progression of diabetic renal fibrosis by restoring autophagy via regulating Keap1/Nrf2 pathway.
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