ArticleFrontiers in physiology2017
Empagliflozin Limits Myocardial Infarction
Article in Frontiers in physiology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to 2 registered trials, which are not on this map. Cited by 93 papers, 2 of them syntheses that pooled it.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Dapagliflozin to Prevent Atrial Fibrillation Recurrence After Transcatheter Pulmonary Venous Isolation.
Clinical Study on Reducing Myocardial Infarction Siez After Primary PCI in Patients With ST Segment Elevation Myocardial Infarction by Using Henagliflozin
Who cites it
93 citing papers in PubMed, 2 syntheses or guidelines pooled it, 154 citations in OpenAlex.
- Sodium-glucose cotransporter 2 inhibitors reduce myocardial infarct size in preclinical animal models of myocardial ischaemia-reperfusion injury: a meta-analysis.Diabetologia · 2021Pooled it
- Practical guidelines for rigor and reproducibility in preclinical and clinical studies on cardioprotection.Basic research in cardiology · 2018Guideline
- Effects of empagliflozin versus placebo on cardiac sympathetic activity in acute myocardial infarction patients with type 2 diabetes mellitus: the EMBODY trial.Cardiovascular diabetology · 2020 · on this mapTrial
- Effects of Glucagon-Like Peptide-1 Receptor Agonists, Sodium-Glucose Cotransporter-2 Inhibitors, and Their Combination on Endothelial Glycocalyx, Arterial Function, and Myocardial Work Index in Patients With Type 2 Diabetes Mellitus After 12-Month Treatment.Journal of the American Heart Association · 2020Trial
- How does empagliflozin improve arterial stiffness in patients with type 2 diabetes mellitus? Sub analysis of a clinical trial.Cardiovascular diabetology · 2019Trial
- Preclinical Evaluation of Berry Extracts as a Nutritional Intervention to Alleviate Myocardial Ischemia-Reperfusion Injury and Atherosclerosis Development.Phytotherapy research : PTR · 2026Article
- Organ-Specific Efficacy of Postischemic Empagliflozin in Acute Stroke and Myocardial Infarction Using Preclinical Models.Journal of the American Heart Association · 2026Article
- Insights in ischemia/reperfusion injury and cardioprotection: neglected and emerging pathways and therapeutic targets for a personalized therapy.Basic research in cardiology · 2026Review
- Inhibition of TLR4/TRAF6/NF-κB pathway by empagliflozin mitigates concanavalin A-induced autoimmune hepatitis in mice.Naunyn-Schmiedeberg's archives of pharmacology · 2026Article
- Empagliflozin improves metabolism and prevents myocardial and coronary dysfunction in streptozotocin-diabetic and non-diabetic rats subjected to ischemia/reperfusion.Basic research in cardiology · 2026Article
- Regulation of Endoplasmic Reticulum Stress by Empagliflozin in Doxorubicin-Induced Cardiotoxicity in Rats.Journal of cellular and molecular medicine · 2026Article
- Sweet relief: exploring mechanisms and therapeutic approaches of sodium-glucose cotransporter-2 inhibitors in cardiovascular-kidney metabolic syndrome.Cardiovascular diabetology · 2026Review
- The value of targeting ketone body metabolism in inflammatory and autoimmune diseases.Journal of translational medicine · 2026Review
- [Association of sodium-glucose linked transporter 2 inhibitors with functional outcomes at discharge in diabetic patients with acute ischemic stroke].Zhejiang da xue xue bao. Yi xue ban = Journal of Zhejiang University. Medical sciences · 2026Article
- The SGLT2 inhibitor empagliflozin promotes increased fatty acid oxidation in skeletal muscle cells.Naunyn-Schmiedeberg's archives of pharmacology · 2026Article
- Identification of Bioactive Ingredients and Mechanistic Pathways of Xuefu Zhuyu Decoction in Ventricular Remodeling: A Network Pharmacology, Molecular Docking and Molecular Dynamics Simulations.Current pharmaceutical design · 2026Article
- Effect of empagliflozin on reducing the no-reflow phenomenon in patients with ST-elevation myocardial infarction: rationale and design of the EMPA-PCI trial.European heart journal open · 2025Article
- The use of SGLT2 inhibitors in older people: What is important?Aging clinical and experimental research · 2025Review
- Empagliflozin restores cardiac metabolism and suppresses immune activation in acute myocardial infarction.Atherosclerosis · 2025Article
- Review
33 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
15 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Empagliflozin (EMPA), a drug approved for type 2 diabetes management, reduced cardiovascular death but is unknown if it reduces myocardial infarction. We sought to investigate: (i) the effect of EMPA on myocardial function and infarct size after ischemia/reperfusion in mice fed with western diet (WD), (ii) the underlying signaling pathways, (iii) its effects on cell survival in rat embryonic-heart-derived cardiomyoblasts (H9C2) and endothelial cells (ECs). To facilitate the aforementioned aims, mice were initially randomized in Control and EMPA groups and were subjected to 30 min ischemia and 2 h reperfusion. EMPA reduced body weight, blood glucose levels, and mean arterial pressure. Cholesterol, triglyceride, and AGEs remained unchanged. Left ventricular fractional shortening was improved (43.97 ± 0.92 vs. 40.75 ± 0.61%) and infarct size reduced (33.2 ± 0.01 vs. 17.6 ± 0.02%). In a second series of experiments, mice were subjected to the above interventions up to the 10th min of reperfusion and myocardial biopsies were obtained for assessment of the signaling cascade. STAT3 was increased in parallel with reduced levels of malondialdehyde (MDA) and reduced expression of myocardial iNOS and interleukin-6. Cell viability and ATP content were increased in H9C2 and in ECs. While, STAT3 phosphorylation is known to bestow infarct sparing properties through interaction with mitochondria, we observed that EMPA did not directly alter the mitochondrial calcium retention capacity (CRC); therefore, its effect in reducing myocardial infarction is STAT3 dependent. In conclusion, EMPA improves myocardial function and reduces infarct size as well as improves redox regulation by decreasing iNOS expression and subsequently lipid peroxidation as shown by its surrogate marker MDA. The mechanisms of action implicate the activation of STAT3 anti-oxidant and anti-inflammatory properties.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.