Evidence map›Paper›PMID 27999547›Full record

ArticleFrontiers in physiology2016

Myocardial Contractile Dysfunction Is Present without Histopathology in a Mouse Model of Limb-Girdle Muscular Dystrophy-2F and Is Prevented after Claudin-5 Virotherapy.

Nima Milani-Nejad, Eric J Schultz, Jessica L Slabaugh, Paul M L Janssen, Jill A Rafael-Fortney

Open access · goldAbstract read
In one paragraph

Article in Frontiers in physiology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
0.5field-weighted citation impact, top 27% of its field
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

2 citing papers in PubMed, 5 citations in OpenAlex.

  1. Discovery ofDiagnostics (Basel, Switzerland) · 2025
    Article
  2. Article
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

5 authors at 1 institution in 1 country.

Nima Milani-NejadDepartment of Physiology and Cell Biology, The Ohio State University Wexner Medical CenterColumbus, OH, USA; Dorothy M. Davis Heart and Lung Research Institute, The Ohio State University Wexner Medical CenterColumbus, OH, USA; Medical Scientist Training Program and Biomedical Sciences Graduate Program, The Ohio State University Wexner Medical CenterColumbus, OH, USA.
Eric J SchultzDepartment of Physiology and Cell Biology, The Ohio State University Wexner Medical CenterColumbus, OH, USA; Dorothy M. Davis Heart and Lung Research Institute, The Ohio State University Wexner Medical CenterColumbus, OH, USA; Department of Molecular and Cellular Biochemistry, The Ohio State University Wexner Medical CenterColumbus, OH, USA.
Jessica L SlabaughDepartment of Physiology and Cell Biology, The Ohio State University Wexner Medical CenterColumbus, OH, USA; Dorothy M. Davis Heart and Lung Research Institute, The Ohio State University Wexner Medical CenterColumbus, OH, USA.
Paul M L JanssenDepartment of Physiology and Cell Biology, The Ohio State University Wexner Medical CenterColumbus, OH, USA; Dorothy M. Davis Heart and Lung Research Institute, The Ohio State University Wexner Medical CenterColumbus, OH, USA.
Jill A Rafael-FortneyDepartment of Physiology and Cell Biology, The Ohio State University Wexner Medical CenterColumbus, OH, USA; Dorothy M. Davis Heart and Lung Research Institute, The Ohio State University Wexner Medical CenterColumbus, OH, USA; Department of Molecular and Cellular Biochemistry, The Ohio State University Wexner Medical CenterColumbus, OH, USA.
The Ohio State University Wexner Medical Center · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Mutations in several members of the dystrophin glycoprotein complex lead to skeletal and cardiomyopathies. Cardiac care for these muscular dystrophies consists of management of symptoms with standard heart medications after detection of reduced whole heart function. Recent evidence from both Duchenne muscular dystrophy patients and animal models suggests that myocardial dysfunction is present before myocardial damage or deficiencies in whole heart function, and that treatment prior to heart failure symptoms may be beneficial. To determine whether this same early myocardial dysfunction is present in other muscular dystrophy cardiomyopathies, we conducted a physiological assessment of cardiac function at the tissue level in the δ-sarcoglycan null mouse model (

Indexed as

cardiac contractile forceclaudin-5heartmuscular dystrophysarcoglycan

Identifiers

PMID27999547
PMCPMC5138189
OpenAlexW2560515651

What OpenQuestion holds

Textmetadata
LicenceCC BY
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 OpenQuestion graph.