ArticleDiabetes, metabolic syndrome and obesity : targets and therapy2020
Empagliflozin Protects Against Proximal Renal Tubular Cell Injury Induced by High Glucose via Regulation of Hypoxia-Inducible Factor 1-Alpha.
Article in Diabetes, metabolic syndrome and obesity : targets and therapy, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
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29 citing papers in PubMed, 43 citations in OpenAlex.
- SGLT2 inhibitors in autosomal dominant polycystic kidney disease: rationale, evidence gaps, and ongoing clinical trials.International urology and nephrology · 2026Review
- Sodium-Glucose Cotransporter 2 Inhibitors in Autosomal Dominant Polycystic Kidney Disease: Mechanistic Insights and Therapeutic Promise.Journal of the American Society of Nephrology : JASN · 2026Review
- Renin-Angiotensin System Inhibitors in Patients With Nonproteinuric Chronic Kidney Disease and Kidney Outcomes: Findings From the CRIC Study.Kidney medicine · 2026Article
- Angiotensin receptor blocker ameliorates the development of tubulointerstitial injury and fibrosis associated with tubular proteinuria observed in subclinical diabetic kidney disease.Frontiers in pharmacology · 2026Article
- Targeting Neurodegeneration with SGLT2is: From Molecular Mechanisms to Clinical Implications.Molecular neurobiology · 2025Review
- The role of hypoxia-inducible factors 1 and 2 in the pathogenesis of diabetic kidney disease.Journal of nephrology · 2025Review
- Research progress of hypoxia-inducible factor-1α and zinc in the mechanism of diabetic kidney disease.Frontiers in pharmacology · 2025Review
- SGLT2 inhibitor downregulates ANGPTL4 to mitigate pathological aging of cardiomyocytes induced by type 2 diabetes.Cardiovascular diabetology · 2024Article
- Is There a Role for SGLT2 Inhibitors in Patients with End-Stage Kidney Disease?Current hypertension reports · 2024Review
- Review
- Exploring Promising Therapies for Non-Alcoholic Fatty Liver Disease: A ClinicalTrials.gov Analysis.Diabetes, metabolic syndrome and obesity : targets and therapy · 2024Review
- Comparative Safety Analysis of Empagliflozin in Type 2 Diabetes Mellitus Patients with Chronic Kidney Disease versus Normal Kidney Function: A Nationwide Cohort Study in Korea.Pharmaceutics · 2023Article
- Empagliflozin improves renal ischemia-reperfusion injury by reducing inflammation and enhancing mitochondrial fusion through AMPK-OPA1 pathway promotion.Cellular & molecular biology letters · 2023Article
- Advances in understanding and treating diabetic kidney disease: focus on tubulointerstitial inflammation mechanisms.Frontiers in endocrinology · 2023Review
- Dapagliflozin Prevents High-Glucose-Induced Cellular Senescence in Renal Tubular Epithelial Cells.International journal of molecular sciences · 2022Article
- Molecular Mechanisms Linking Empagliflozin to Renal Protection in the LLC-PK1 Model of Diabetic Nephropathy.Biomedicines · 2022Article
- Canagliflozin mitigates ferroptosis and ameliorates heart failure in rats with preserved ejection fraction.Naunyn-Schmiedeberg's archives of pharmacology · 2022Article
- Potential Molecular Mechanism of Yishen Capsule in the Treatment of Diabetic Nephropathy Based on Network Pharmacology and Molecular Docking.Diabetes, metabolic syndrome and obesity : targets and therapy · 2022Article
- Renoprotective Role of Hypoxia-Inducible Factors and the Mechanism.Kidney diseases (Basel, Switzerland) · 2022Review
- Transcription Factor ChREBP Mediates High Glucose-Evoked Increase in HIF-1α Content in Epithelial Cells of Renal Proximal Tubules.International journal of molecular sciences · 2021Article
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundEvidence from both animal and human studies clearly supports the renal beneficial effects of empagliflozin (emp), a sodium glucose co-transporter 2 (SGLT2) inhibitor, but the mechanism in which it exerts its effect is not well understood. In this study, we investigated the capability of emp on reducing hyperglycemia-induced renal proximal tubular epithelial cells injury and we evaluated if the renoprotective effect of emp associates with hypoxia-inducible factor-1α (HIF-1α). MATERIALS AND
methodsHuman kidney cell lines (HK-2 cells) were incubated in normoxia, high glucose with or without emp treatment for 72 hours to evaluate the induction of HIF-1α, glucose transporter-1, SGLT2, the fibrosis signal pathway and epithelial-mesenchymal transition (EMT) markers.
resultsHigh glucose (HG) increased expression of Collagen IV, Fibronectin, transforming growth factor-beta1 (TGF-β1). However, emp treatment remarkably decreased expression of TGF-β1, accumulation of extracellular matrix proteins (Fibronectin, Collagen IV), as well as (phosphorylated-smad3) P-smad3. HG increased SGLT2 protein expression compared to normal glucose (NG) while emp significantly decreased SGLT2 expression. Furthermore, emp decreased high glucose-induced alpha-smooth muscle actin (α-SMA) expression and reversed epithelial marker (E-catherin) suppression induced by high glucose. In addition, emp treatment for 72 h increased expression of HIF-1α protein (95% CI: -0.5918 to -0.002338, at 100nM, P < 0.05, 95% CI -0.6631 to -0.07367 at 500nM, P < 0.05) in hyperglycemic normoxic HK-2 cells. Furthermore, we observed increased expression of GLUT-1 protein after emp treatment and remarkably decreased cell proliferation.
conclusionEmp treatment protected proximal renal tubular cells injury induced by high glucose. Induction of HIF-1α expression by emp may play an essential role in the protection of high glucose-induced proximal renal tubular epithelial cells injury.
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