ArticleAmerican journal of physiology. Heart and circulatory physiology2024
Empagliflozin treatment rescues abnormally reduced Na
Article in American journal of physiology. Heart and circulatory physiology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 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
13 citing papers in PubMed, 13 citations in OpenAlex.
- Repurposing Empagliflozin for Duchenne Muscular Dystrophy-Associated Cardiomyopathy: Protocol for a Pharmacokinetics, Safety and Proof-of-Concept Trial in Children.Cardiology and therapy · 2026Article
- Cardiac Medication Use in ACTION for Duchenne Muscular Dystrophy Cardiomyopathy.Pediatric cardiology · 2026Article
- Empagliflozin preserves cardiac function and modulates metabolism in a mouse model of Duchenne muscular dystrophy.bioRxiv : the preprint server for biology · 2026Article
- Molecular Mechanisms and Therapeutic Strategies in Heart Failure Due to Dystrophin Deficiency: A Comprehensive Review.Reviews in cardiovascular medicine · 2026Review
- Targeting Skeletal Muscle in Duchenne Muscular Dystrophy: Integrating in Silico and Experimental Approaches to Sodium-Glucose Cotransporter-2 Inhibition.The American journal of pathology · 2026Article
- Investigating Sodium-Glucose Cotransporter 2 Inhibitors Versus Other Glucose-Lowering Drugs on Ventricular Arrhythmias or Sudden Cardiac Death Using the US FDA Adverse Event Reporting System.Cardiovascular drugs and therapy · 2025Article
- SGLT2 inhibitors to the rescue: restoring cardiac sodium channel membrane function in muscular dystrophy.American journal of physiology. Heart and circulatory physiology · 2025Article
- Translational progress in the development of pharmacotherapies for Duchenne muscular dystrophy.Regenerative medicine · 2025Article
- The sodium/glucose cotransporter 2 inhibitor empagliflozin is a pharmacological chaperone of cardiac NaAmerican journal of physiology. Heart and circulatory physiology · 2025Article
- Propionic Acidemia-Induced Proarrhythmic Electrophysiological Alterations in Human iPSC-Derived Cardiomyocytes.Journal of inherited metabolic disease · 2025Article
- SGLT2 inhibitors: how do they affect the cardiac cells.Molecular and cellular biochemistry · 2025Review
- Conduction defects and arrhythmias inFrontiers in physiology · 2025Article
- Cell size induced bias of current density in hypertrophic cardiomyocytes.Channels (Austin, Tex.) · 2024Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
11 authors at 1 institution in 1 country.
Funding
Abstract
Cardiac arrhythmias significantly contribute to mortality in Duchenne muscular dystrophy (DMD), a severe muscle illness caused by mutations in the gene encoding for the intracellular protein dystrophin. A major source for arrhythmia vulnerability in patients with DMD is impaired ventricular impulse conduction, which predisposes for ventricular asynchrony, decreased cardiac output, and the development of reentrant circuits. Using the dystrophin-deficient
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.