Evidence map›Paper›PMID 22547149›Full record

ArticleMolecular therapy : the journal of the American Society of Gene Therapy2012

Sustaining cardiac claudin-5 levels prevents functional hallmarks of cardiomyopathy in a muscular dystrophy mouse model.

Dawn A Delfín, Ying Xu, Kevin E Schill, Tessily A Mays, Benjamin D Canan, Kara E Zang, Jamie A Barnum, Paul M L Janssen, Jill A Rafael-Fortney

Open access · bronzeAbstract read
In one paragraph

Article in Molecular therapy : the journal of the American Society of Gene Therapy, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
0.5field-weighted citation impact, top 36% 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

16 citing papers in PubMed, 24 citations in OpenAlex.

  1. Article
  2. Review
  3. Discovery ofDiagnostics (Basel, Switzerland) · 2025
    Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Review
  10. Claudin-5: gatekeeper of neurological function.Fluids and barriers of the CNS · 2019
    Review
  11. Article
  12. Article
  13. Article
  14. Treatment of dystrophin cardiomyopathies.Nature reviews. Cardiology · 2014
    Review
  15. Review
  16. Claudin-5 levels are reduced from multiple cell types in human failing hearts and are associated with mislocalization of ephrin-B1.Cardiovascular pathology : the official journal of the Society for Cardiovascular Pathology
    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

9 authors at 1 institution in 1 country.

Dawn A DelfínDepartment of Molecular and Cellular Biochemistry, College of Medicine, The Ohio State University, Columbus, Ohio 43210, USA.
Ying Xu
Kevin E Schill
Tessily A Mays
Benjamin D Canan
Kara E Zang
Jamie A Barnum
Paul M L Janssen
Jill A Rafael-Fortney
The Ohio State University · US

Funding

Training in Congenital and Acquired Heart DiseaseT32HL098039 · NHLBI · RESEARCH INST NATIONWIDE CHILDREN'S HOSP · PI GARG, VIDU, MOHLER, PETER J. · 2009 to 2019
$2.5M
NHLBI NIH HHS T32 HL098039
6 · The paper itself

Abstract

Identification of new molecular targets in heart failure could ultimately have a substantial positive impact on both the health and financial aspects of treating the large heart failure population. We originally identified reduced levels of the cell junction protein claudin-5 specifically in heart in the dystrophin/utrophin-deficient (Dmd(mdx);Utrn(-/-)) mouse model of muscular dystrophy and cardiomyopathy, which demonstrates physiological hallmarks of heart failure. We then showed that at least 60% of cardiac explant samples from patients with heart failure resulting from diverse etiologies also have reduced claudin-5 levels. These claudin-5 reductions were independent of changes in other cell junction proteins previously linked to heart failure. The goal of this study was to determine whether sustaining claudin-5 levels is sufficient to prevent the onset of histological and functional indicators of heart failure. Here, we show the proof-of-concept rescue experiment in the Dmd(mdx);Utrn(-/-) model, in which claudin-5 reductions were originally identified. Expression of claudin-5 4 weeks after a single administration of recombinant adeno-associated virus (rAAV) containing a claudin-5 expression cassette prevented the onset of physiological hallmarks of cardiomyopathy and improved histological signs of cardiac damage. This experiment demonstrates that claudin-5 may represent a novel treatment target for prevention of heart failure.

Indexed as

AnimalsCardiomyopathiesClaudin-5DependovirusDisease Models, AnimalDystrophinGene Transfer TechniquesHeart FailureMiceMice, Inbred C57BLMice, TransgenicMuscular Dystrophy, AnimalMyocardiumUtrophinapo-dystrophin 1Claudin-5Cldn5 protein, mouseDystrophinUtrn protein, mouseUtrophin

Identifiers

PMID22547149
PMCPMC3392970
OpenAlexW1971156867

What OpenQuestion holds

Textmetadata
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.