ArticleToxicology research2023
Empagliflozin attenuates doxorubicin-induced cardiotoxicity by activating AMPK/SIRT-1/PGC-1α-mediated mitochondrial biogenesis.
Article in Toxicology research, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
30 citing papers in PubMed, 36 citations in OpenAlex.
- Empagliflozin Attenuates Cardiac Dysfunction in Rat Model of Metabolic Syndrome: Evaluating Role of the Cardiac Renin-Angiotensin System.Biomedicines · 2026Article
- Empagliflozin Protects Against Doxorubicin Cardiotoxicity: Integrative Assessment of Cardiac Kinetics and Electrophysiology Using Machine Learning in a Rat Model.Medical sciences (Basel, Switzerland) · 2026Article
- Class Effect of SGLT2 Inhibitors Against Doxorubicin-Induced Cardiotoxicity via Regulating Adenosine Kinase Mediated-Cardiac Oxidative Stress.Cardiovascular drugs and therapy · 2026Article
- Cardiotoxicity induced by multiple myeloma therapies: mechanistic convergence across proteasome inhibitors, CAR-T, and bispecific antibodies.Blood cancer journal · 2026Review
- Ginkgetin Alleviates Doxorubicin-Induced Heart Failure by Regulating Mitochondrial Dysfunction Through the AMPK/Sirt1/NF-κB Signaling Pathway.Balkan medical journal · 2026Article
- Empagliflozin Mitigates Doxorubicin-Induced Cardiotoxicity in Rats: Electrocardiographic, Biochemical, and Histopathological Evidence.International journal of molecular sciences · 2026Article
- Role of solute carrier transporters in the biodistribution and toxicity of chemotherapeutic drugs.Pharmacological reviews · 2026Review
- Diabetes and cancer: therapeutic implications.Cardio-oncology (London, England) · 2026Review
- Mitochondrial dysfunction-driven PANoptosis in doxorubicin-induced cardiotoxicity: mechanistic insights and intervention strategies.Frontiers in pharmacology · 2026Review
- Pharmacological prevention in cardio-oncology: from bench-to-bedside.Heart failure reviews · 2025Review
- Deletion of cardiac fibroblast growth factor-23 beneficially impacts myocardial energy metabolism in left ventricular hypertrophy.npj metabolic health and disease · 2025Article
- Association between sodium-glucose co-transporter-2 inhibitors and cardiac outcomes in cancer patients: a systematic review and meta-analysis.Journal of geriatric cardiology : JGC · 2025Article
- Empagliflozin Protects Against Oxidative Stress in the Diabetic Brain by Inducing HPharmaceuticals (Basel, Switzerland) · 2025Article
- Potential New Applications of Sodium-Glucose Cotransporter-2 Inhibitors Across the Continuum of Cancer-Related Cardiovascular Toxicity.Pharmaceuticals (Basel, Switzerland) · 2025Review
- Sodium-Glucose Cotransporter 2 Inhibitors in Aortic Stenosis: Toward a Comprehensive Cardiometabolic Approach.International journal of molecular sciences · 2025Review
- Doxorubicin-Induced Cardiotoxicity and the Emerging Role of SGLT2 Inhibitors: From Glycemic Control to Cardio-Oncology.Pharmaceuticals (Basel, Switzerland) · 2025Review
- Article
- Single cell transcriptomic analysis of SGLT2 expression supports an indirect or off-target role for the cardioprotective benefits of empagliflozin in heart failure.Scientific reports · 2025Article
- SGLT2 inhibitors for prevention and management of cancer treatment-related cardiovascular toxicity: a review of potential mechanisms and clinical insights.Cardio-oncology (London, England) · 2025Review
- SGLT2 Inhibitors in Combination Therapies for Tumors: A Novel Approach to Synergistic Treatment Strategies.Drug design, development and therapy · 2025Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
1 author at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
We aimed to probe the functions and possible mechanisms of empagliflozin in doxorubicin (Dox)-caused cardiotoxicity. First, a cardiotoxicity rat model was built by continuously injecting Dox intraperitoneally. Then, empagliflozin (30 mg/kg) was gavaged into the rats. Next, echocardiography was utilized for checking the cardiac function of rats, and H&E staining for observing pathological alterations of the myocardial tissues. Besides, biochemical assays and Enzyme-linked Immunosorbent Assay were adopted to detect the creatine kinase isoenzyme (CK-MB), N-terminal pro-brain natriuretic peptide (NT-proBNP), adenosine triphosphate (ATP), adenosine diphosphate (ADP), and adenosine monophosphate (AMP) levels in rat serum and superoxide dismutase (SOD), malondialdehyde acid (MDA), and catalase (CAT) in myocardial tissue, respectively. Furthermore, the expression of AMPK/SIRT-1/PGC-1α signaling pathway-related proteins in the myocardial tissues was tested by Western blot. Continuous intraperitoneal injection of Dox greatly elevated left ventricular end-systolic diameter (LVESD) and left ventricular end-diastolic diameter (LVEDD), reduced fractional shortening (FS) and ejection fraction (EF), and notably up-regulated CK-MB and NT-proBNP level in rats' serum, thus impairing cardiac function. Empagliflozin treatment could ameliorate myocardial histopathological damage and alleviate cardiac function and tissue damage by down-regulating LVEDD and LVESD, up-regulating EF and FS, and inhibiting CK-MB and NT-proBNP level in serum. Additionally, empagliflozin improved Dox-induced excessive oxidative stress and dysregulation of energy metabolism. Furthermore, empagliflozin activated the AMPK/SIRT-1/PGC-1α signaling pathway in Dox-caused cardiotoxicity rats. In conclusion, in addition to bettering the cardiac tissue and function injury caused by Dox, empagliflozin also improves excessive oxidative stress and energy metabolism. Notably, empagliflozin may exert cardioprotective effects through activating the AMPK/SIRT-1/PGC-1α pathway.
Indexed as
Identifiers
What OpenQuestion holds
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.