Evidence map›Paper›PMID 41959027›Full record

ArticlebioRxiv : the preprint server for biology2026

Empagliflozin preserves cardiac function and modulates metabolism in a mouse model of Duchenne muscular dystrophy.

Benjamin J Zeidler, Connor Thomas, John P Salvas, Areli Jannes S Javier, Alyssa M Richards, Linda A Bean, Conner C Earl, Akanksha Agrawal, Niharika Narra, Lifan Zeng and 8 more

Abstract readPreprint
PubMed Full text at PMC Publisher
In one paragraph

Article in bioRxiv : the preprint server for biology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

0 citing papers in PubMed.

No citing paper in PubMed yet.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

18 authors.

Benjamin J ZeidlerWeldon School of Biomedical Engineering, Purdue University, West Lafayette, IN.
Connor ThomasDepartment of Anatomy, Cell Biology & Physiology, Indiana University School of Medicine, Indianapolis, IN.
John P SalvasWeldon School of Biomedical Engineering, Purdue University, West Lafayette, IN.
Areli Jannes S JavierIndiana Center for Musculoskeletal Health, Indiana University School of Medicine, Indianapolis, IN.
Alyssa M RichardsWeldon School of Biomedical Engineering, Purdue University, West Lafayette, IN.
Linda A BeanDepartment of Anatomy, Cell Biology & Physiology, Indiana University School of Medicine, Indianapolis, IN.
Conner C EarlWeldon School of Biomedical Engineering, Purdue University, West Lafayette, IN.
Akanksha AgrawalDepartment of Anatomy, Cell Biology & Physiology, Indiana University School of Medicine, Indianapolis, IN.
Niharika NarraWeldon School of Biomedical Engineering, Purdue University, West Lafayette, IN.
Lifan ZengChemical Genomics Core Facility, Department of Biochemistry, Molecular Biology and Pharmacology, Indiana University School of Medicine, Indianapolis, IN.
Carol A WitczakDepartment of Anatomy, Cell Biology & Physiology, Indiana University School of Medicine, Indianapolis, IN.
Joshua R HuotDepartment of Anatomy, Cell Biology & Physiology, Indiana University School of Medicine, Indianapolis, IN.
Il-Man KimDepartment of Anatomy, Cell Biology & Physiology, Indiana University School of Medicine, Indianapolis, IN.
Meena S MadhurDepartment of Medicine, Indiana University School of Medicine, Indianapolis, IN.
Mark C KowalaDepartment of Medicine, Indiana University School of Medicine, Indianapolis, IN.
Larry W MarkhamDepartment of Medicine, Indiana University School of Medicine, Indianapolis, IN.
Craig J GoergenWeldon School of Biomedical Engineering, Purdue University, West Lafayette, IN.ORCID 0000-0001-8883-7953
Steven S WelcDepartment of Anatomy, Cell Biology & Physiology, Indiana University School of Medicine, Indianapolis, IN.ORCID 0000-0002-2353-0325

Funding

Comprehensive Training Program in Musculoskeletal ResearchT32AR065971 · NIAMS · INDIANA UNIVERSITY INDIANAPOLIS · PI ALEXANDER G ROBLING · 2015 to 2026
$4.4M
Paracrine actions of fibroblasts promote pathologic cardiac myocyte remodeling in Duchenne muscular dystrophyR01HL158647 · NHLBI · INDIANA UNIVERSITY INDIANAPOLIS · PI WELC, STEVEN S · 2021 to 2025
$2.6M
Modeling Mortality in Duchenne Muscular Dystrophy Cardiomyopathy: Identification of Surrogate Outcome Measures for DMD Drug TrialsR01HL167969 · NHLBI · VANDERBILT UNIVERSITY MEDICAL CENTER · PI Craig J. Goergen, Kan N Hor · 2024 to 2026
$2.3M
Deciphering the novel regulatory mechanisms of neovascularization, cardiomyocyte survival, and endothelial cell-cardiomyocyte crosstalk in myocardial infarctionR01HL180692 · NHLBI · INDIANA UNIVERSITY INDIANAPOLIS · PI Il-man Kim · 2025 to 2026
$1.3M
NHLBI NIH HHS R01 HL158647NHLBI NIH HHS R01 HL167969NHLBI NIH HHS R01 HL180692NIAMS NIH HHS T32 AR065971
6 · The paper itself

Abstract

Duchenne muscular dystrophy (DMD) is a fatal genetic disorder characterized by skeletal muscle degeneration and cardiomyopathy without a cure. This study examined the therapeutic potential of the sodium-glucose cotransporter 2 (SGLT2) inhibitor empagliflozin (EMPA) on cardiac function in the dystrophin-deficient

Identifiers

PMID41959027
PMCPMC13060957

What Socratic holds

Textmetadata
LicenceCC BY-NC-ND
Read underepoch 390

Registered trials

None linked

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 Socratic graph.