ArticleScientific reports2021
Empagliflozin maintains capillarization and improves cardiac function in a murine model of left ventricular pressure overload.
Article in Scientific reports, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.
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Who cites it
31 citing papers in PubMed, 41 citations in OpenAlex.
- Empagliflozin Improves Endothelial Function in an Ovariectomized Rat Model of Estrogen Deficiency.Journal of cardiovascular translational research · 2026Article
- Angiogenic Potential of Endothelial Cells in Response to the Stiffness and Anisotropy of Right Ventricle Mimetic Scaffolds.Bioengineering (Basel, Switzerland) · 2026Article
- Sodium-glucose Co-transporter 2 (SGLT2) inhibitor dapagliflozin acutely activates cardiomyocyte HIF-1α signaling via succinate, a signaling metabolite.Journal of pharmacological sciences · 2026Article
- Vasculoprotective Effects of Sodium-Glucose Co-Transporter Inhibitors in Non-Diabetic Experimental Settings: A Narrative Review.International journal of molecular sciences · 2026Review
- Empagliflozin Attenuates Cardiac Fibrosis by Suppressing Fibroblast-Mediated C-C Motif Chemokine Ligand 2 Expression.Journal of the American Heart Association · 2026Article
- Myocardial ischemia reperfusion in diabetes: mechanism of injury and its drug treatment.Diabetology & metabolic syndrome · 2026Review
- Effects of SGLT2 inhibitors on angiography-derived coronary microcirculatory resistance and clinical outcomes in patients with coronary heart disease and type 2 diabetes: A cohort study.Diabetology & metabolic syndrome · 2025Article
- Effects of a Novel Mammalian-Derived Collagen Matrix on Human Articular Cartilage-Derived Chondrocytes from Osteoarthritis Patients.International journal of molecular sciences · 2025Article
- Endothelial dysfunction in chronic kidney disease: a clinical perspective.American journal of physiology. Heart and circulatory physiology · 2025Review
- Sodium-glucose cotransporter-2 inhibitors in cardiovascular disease: a gaseous solution.Medical gas research · 2025Article
- Mitochondrial apoptosis in response to cardiac ischemia-reperfusion injury.Journal of translational medicine · 2025Review
- Empagliflozin targeting STAT3/Akt/Nrf2 axis promoting diabetic wound healing in rat model.Frontiers in pharmacology · 2025Article
- Metabolic Syndrome, Kidney-Related Adiposity, and Kidney Microcirculation: Unraveling the Damage.Biomedicines · 2024Review
- The Effects of SGLT2 Inhibitors on Blood Pressure and Other Cardiometabolic Risk Factors.International journal of molecular sciences · 2024 · on this mapReview
- New insights into the cardio-renal benefits of SGLT2 inhibitors and the coordinated role of miR-30 family.Genes & diseases · 2024Review
- SGLT2 Inhibitors and How They Work Beyond the Glucosuric Effect. State of the Art.American journal of cardiovascular drugs : drugs, devices, and other interventions · 2024Review
- Sodium-Glucose Cotransporter 2 Inhibitor Therapy in Different Scenarios of Heart Failure: An Overview of the Current Literature.International journal of molecular sciences · 2024Review
- The potential anti-arrhythmic effect of SGLT2 inhibitors.Cardiovascular diabetology · 2024Review
- Role and molecular mechanisms of SGLT2 inhibitors in pathological cardiac remodeling (Review).Molecular medicine reports · 2024Review
- Elucidating the cardioprotective mechanisms of sodium-glucose cotransporter-2 inhibitors beyond glycemic control.World journal of diabetes · 2024Article
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Authors and funding
11 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Patients with type 2 diabetes treated with Sodium glucose transporter 2 (SGLT2) inhibitors show reduced mortality and hospitalization for heart failure (HF). SGLT2 inhibitors are considered to activate multiple cardioprotective pathways; however, underlying mechanisms are not fully described. This study aimed to elucidate the underlying mechanisms of the beneficial effects of SGLT2 inhibitors on the failing heart. We generated a left ventricular (LV) pressure overload model in C57BL/6NCrSlc mice by transverse aortic constriction (TAC) and examined the effects of empagliflozin (EMPA) in this model. We conducted metabolome and transcriptome analyses and histological and physiological examinations. EMPA administration ameliorated pressure overload-induced systolic dysfunction. Metabolomic studies showed that EMPA increased citrulline levels in cardiac tissue and reduced levels of arginine, indicating enhanced metabolism from arginine to citrulline and nitric oxide (NO). Transcriptome suggested possible involvement of the insulin/AKT pathway that could activate NO production through phosphorylation of endothelial NO synthase (eNOS). Histological examination of the mice showed capillary rarefaction and endothelial apoptosis after TAC, both of which were significantly improved by EMPA treatment. This improvement was associated with enhanced expression phospho-eNOS and NO production in cardiac endothelial cells. NOS inhibition attenuated these cardioprotective effects of EMPA. The in vitro studies showed that catecholamine-induced endothelial apoptosis was inhibited by NO, arginine, or AKT activator. EMPA activates the AKT/eNOS/NO pathway, which helps to suppress endothelial apoptosis, maintain capillarization and improve systolic dysfunction during LV pressure overload.
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