ArticleFrontiers in pharmacology2022
Atorvastatin Restores PPARα Inhibition of Lipid Metabolism Disorders by Downregulating miR-21 Expression to Improve Mitochondrial Function and Alleviate Diabetic Nephropathy Progression.
Article in Frontiers in pharmacology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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17 citing papers in PubMed.
- Psoralen enhances direct cardiac reprogramming via activating PPARα and driving mitochondrial fission and improves cardiac function after myocardial infarction.Stem cell research & therapy · 2026Article
- Abnormal lipid metabolism in senescent renal tubular cells in diabetic nephropathy.Cellular and molecular life sciences : CMLS · 2026Review
- Roles of the peroxisome proliferator-activated receptors (PPARs) in the pathogenesis of diabetic kidney disease (DKD).Cell death discovery · 2026Review
- Evaluation of the anti-inflammatory potential of atorvastatin targeting TNF-α, IL-6, and IL-1β using integrated in vitro and in silico approaches.Scientific reports · 2026Article
- Atorvastatin Attenuates Vancomycin-Induced Nephrotoxicity via PPARα-Associated Regulation of SLC Transporters.Drug design, development and therapy · 2026Article
- Bidirectional regulation between mitochondrial metabolic reprogramming and epigenetic modifications in renal tubular epithelial cell injury of diabetic kidney disease.Frontiers in endocrinology · 2026Review
- Polyphenol-rich Chinese olive extracts attenuate lipid accumulation in HepG2 cells, accompanied by AMPK phosphorylation and miRNA alterations.Frontiers in nutrition · 2026Article
- DeSUMOylation of RBMX regulates exosomal sorting of cargo to promote renal tubulointerstitial fibrosis in diabetic kidney disease.Journal of advanced research · 2025Article
- What a Modern Physician Should Know About microRNAs in the Diagnosis and Treatment of Diabetic Kidney Disease.International journal of molecular sciences · 2025Review
- Targeting microRNAs in diabetic retinopathy: from pathogenic mechanisms to therapeutic potentials.Frontiers in endocrinology · 2025Review
- Chlorogenic acid alleviates renal fibrosis by reducing lipid accumulation in diabetic kidney disease through suppressing the Notch1 and Stat3 signaling pathway.Renal failure · 2024Article
- Effect of Atorvastatin combined with Irbesartan in the treatment of early diabetic nephropathy.Pakistan journal of medical sciences · 2024Article
- Roles of Mitochondrial Dysfunction in Diabetic Kidney Disease: New Perspectives from Mechanism to Therapy.Biomolecules · 2024Review
- Broadening Horizons: Exploring mtDAMPs as a Mechanism and Potential Intervention Target in Cardiovascular Diseases.Aging and disease · 2023Review
- MicroRNA-21 Silencing in Diabetic Nephropathy: Insights on Therapeutic Strategies.Biomedicines · 2023Review
- Formononetin Attenuates Renal Tubular Injury and Mitochondrial Damage in Diabetic Nephropathy Partly via Regulating Sirt1/PGC-1α Pathway.Frontiers in pharmacology · 2022Article
- Senescent renal tubular epithelial cells activate fibroblasts by secreting Shh to promote the progression of diabetic kidney disease.Frontiers in medicine · 2022Article
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13 authors.
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Abstract
Atorvastatin is a classical lipid-lowering drug. It has been reported to have renoprotective effects, such as reducing urinary protein excretion and extracellular matrix aggregation. The present study aimed to investigate the specific mechanism of action of Atorvastatin in type 1 diabetic mice (T1DM) in inhibiting renal tubular epithelial cell injury following treatment with high glucose and high fat. The anti-injury mechanism of Atorvastatin involved the inhibition of miR-21 expression and the upregulation of the transcription and expression of its downstream gene Peroxisome proliferator-activated receptors-α(PPARα). An increase in blood glucose and lipid levels was noted in the T1DM model, which was associated with renal fibrosis and inflammation. These changes were accompanied by increased miR-21 levels, downregulation of PPARα and Mfn1 expressions, and upregulation of Drp1 and IL6 expressions in renal tissues. These phenomena were reversed following the administration of Atorvastatin. miR-21 targeted PPARα by inhibiting its mRNA translation. Inhibition of miR-21 expression or Fenofibrate (PPARα agonist) administration prevented the decrease of PPARα in renal tubular epithelial cells under high glucose (HG) and high fat (Palmitic acid, PA) conditions, alleviating lipid metabolism disorders and reducing mitochondrial dynamics and inflammation. Consistent with the
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