ArticleInternational journal of molecular sciences2021
Empagliflozin Ameliorates Free Fatty Acid Induced-Lipotoxicity in Renal Proximal Tubular Cells via the PPARγ/CD36 Pathway in Obese Mice.
Article in International journal of molecular sciences, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers, 1 of them a synthesis that pooled it.
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Who cites it
33 citing papers in PubMed, 1 synthesis or guideline pooled it, 44 citations in OpenAlex.
- Lipid homeostasis in diabetic kidney disease.International journal of biological sciences · 2024Pooled it
- Review
- Abnormal lipid metabolism in senescent renal tubular cells in diabetic nephropathy.Cellular and molecular life sciences : CMLS · 2026Review
- More than Glucose Elimination: Additional Benefits of SGLT2 Inhibitors in Glomerular Diseases.Drugs · 2026Review
- Tubulointerstitial inflammation and fibrosis induced by proteinuria: fresh insights.Frontiers in pharmacology · 2026Review
- Empagliflozin attenuates dexamethasone-induced non-alcoholic steatohepatitis by regulation of ferroptosis, inflammation and autophagy.Frontiers in pharmacology · 2026Article
- Ectopic lipid deposition in kidney diseases: mechanisms in specific cell types and therapeutic strategies.Frontiers in endocrinology · 2026Review
- Age-adjusted visceral adiposity index as a predictor of chronic kidney disease: insights from NHANES 2007-2018.Renal failure · 2025Article
- Evaluation of Serum Soluble CD36 Levels in the Clinical Progression of Diabetic Nephropathy.EJIFCC · 2025Article
- Noninvasive assessment of metabolic syndrome-related renal injury using magnetic resonance imaging fat fraction and apparent diffusion coefficient: A cross-sectional study.The Journal of international medical research · 2025Article
- Phillyrin prevents calcium oxalate kidney stones through the PPARγ signaling pathway.Renal failure · 2025Article
- Lipid Accumulation and Insulin Resistance: Bridging Metabolic Dysfunction-Associated Fatty Liver Disease and Chronic Kidney Disease.International journal of molecular sciences · 2025Review
- Research progress in the treatment of lipid metabolism disorder in patients with diabetic kidney disease by the integrated traditional Chinese and Western medicine.Frontiers in endocrinology · 2025Review
- From Adipose to Ailing Kidneys: The Role of Lipid Metabolism in Obesity-Related Chronic Kidney Disease.Antioxidants (Basel, Switzerland) · 2024Review
- The Application of Duck Embryonic Fibroblasts CCL-141 as a Cell Model for Adipogenesis.Animals : an open access journal from MDPI · 2024Article
- Sodium-Glucose Cotransporter Inhibitors: Cellular Mechanisms Involved in the Lipid Metabolism and the Treatment of Chronic Kidney Disease Associated with Metabolic Syndrome.Antioxidants (Basel, Switzerland) · 2024Review
- DACH1 attenuated PA-induced renal tubular injury through TLR4/MyD88/NF-κB and TGF-β/Smad signalling pathway.Journal of endocrinological investigation · 2024Article
- Focus on Mitochondrial Respiratory Chain: Potential Therapeutic Target for Chronic Renal Failure.International journal of molecular sciences · 2024Review
- Empagliflozin improves aortic injury in obese mice by regulating fatty acid metabolism.Open medicine (Warsaw, Poland) · 2024Article
- Improved Glycaemic Control and Nephroprotective Effects of Empagliflozin and Paricalcitol Co-Therapy in Mice with Type 2 Diabetes Mellitus.International journal of molecular sciences · 2023Article
Corrections and comments
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
Abstract
High serum levels of free fatty acids (FFAs) could contribute to obesity-induced nephropathy. CD36, a class B scavenger receptor, is a major receptor mediating FFA uptake in renal proximal tubular cells. Empagliflozin, a new anti-diabetic agent, is a specific inhibitor of sodium-glucose co-transporter 2 channels presented on renal proximal tubular cells and inhibits glucose reabsorption. In addition, empagliflozin has shown renoprotective effects. However, the mechanism through which empagliflozin regulates CD36 expression and attenuates FFA-induced lipotoxicity remains unclear. Herein, we aimed to elucidate the crosstalk between empagliflozin and CD36 in FFA-induced renal injury. C57BL/6 mice fed a high-fat diet (HFD) and palmitic acid-treated HK-2 renal tubular cells were used for in vivo and in vitro assessments. Empagliflozin attenuated HFD-induced body weight gain, insulin resistance, and inflammation in mice. In HFD-fed mice, CD36 was upregulated in the tubular area of the kidney, whereas empagliflozin attenuated CD36 expression. Furthermore, empagliflozin downregulated the expression of peroxisome proliferator-activated receptor (PPAR)-γ. Treatment with a PPARγ inhibitor (GW9662) did not further decrease PPARγ expression, whereas a PPARγ antagonist reversed this effect; this suggested that empagliflozin may, at least partly, decrease CD36 by modulating PPARγ. In conclusion, empagliflozin can ameliorate FFA-induced renal tubular injury via the PPARγ/CD36 pathway.
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