Evidence map›Paper›PMID 21455723›Full record

ArticleBasic research in cardiology2011

Desmoglein 2 mutant mice develop cardiac fibrosis and dilation.

Claudia A Krusche, Bastian Holthöfer, Valérie Hofe, Annette M van de Sandt, Leonid Eshkind, Ernesto Bockamp, Marc W Merx, Sebastian Kant, Reinhard Windoffer, Rudolf E Leube

Open access · bronzeAbstract read
In one paragraph

Article in Basic research in cardiology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers.

0numbers the graph read from it
0cells of the map it votes in
45citing papers in PubMed
4.1field-weighted citation impact, top 6% 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

45 citing papers in PubMed, 84 citations in OpenAlex.

  1. Article
  2. Article
  3. Structural Insights into Ordered Multicomponent Assemblies in Cell Junctions.Advances in experimental medicine and biology · 2026
    Review
  4. Review
  5. Article
  6. Review
  7. Review
  8. Article
  9. Article
  10. Molecular Pathways and Animal Models of Cardiomyopathies.Advances in experimental medicine and biology · 2024
    Article
  11. Review
  12. Review
  13. Article
  14. Article
  15. Article
  16. Review
  17. Article
  18. Article
  19. Review
  20. 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

10 authors at 5 institutions in 1 country.

Claudia A KruscheInstitute of Molecular and Cellular Anatomy, RWTH Aachen University, Wendlingweg 2, Aachen, Germany. ckrusche@ukaachen.de
Bastian Holthöfer
Valérie Hofe
Annette M van de Sandt
Leonid Eshkind
Ernesto Bockamp
Marc W Merx
Sebastian Kant
Reinhard Windoffer
Rudolf E Leube
RWTH Aachen University · DEDüsseldorf University Hospital · DEHeinrich Heine University Düsseldorf · DEJohannes Gutenberg University Mainz · DEUniversity Medical Center of the Johannes Gutenberg University Mainz · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Desmosomes are cell-cell adhesion sites and part of the intercalated discs, which couple adjacent cardiomyocytes. The connection is formed by the extracellular domains of desmosomal cadherins that are also linked to the cytoskeleton on the cytoplasmic side. To examine the contribution of the desmosomal cadherin desmoglein 2 to cardiomyocyte adhesion and cardiac function, mutant mice were prepared lacking a part of the extracellular adhesive domain of desmoglein 2. Most live born mutant mice presented normal overall cardiac morphology at 2 weeks. Some animals, however, displayed extensive fibrotic lesions. Later on, mutants developed ventricular dilation leading to cardiac insufficiency and eventually premature death. Upon histological examination, cardiomyocyte death by calcifying necrosis and replacement by fibrous tissue were observed. Fibrotic lesions were highly proliferative in 2-week-old mutants, whereas the fibrotic lesions of older mutants showed little proliferation indicating the completion of local muscle replacement by scar tissue. Disease progression correlated with increased mRNA expression of c-myc, ANF, BNF, CTGF and GDF15, which are markers for cardiac stress, remodeling and heart failure. Taken together, the desmoglein 2-mutant mice display features of dilative cardiomyopathy and arrhythmogenic right ventricular cardiomyopathy, an inherited human heart disease with pronounced fibrosis and ventricular arrhythmias that has been linked to mutations in desmosomal proteins including desmoglein 2.

Indexed as

AnimalsCardiomegalyDesmoglein 2Dilatation, PathologicFemaleFibrosisGrowth Differentiation Factor 15MaleMiceMice, Inbred C57BLMice, TransgenicMutationMyocardiumDesmoglein 2Dsg2 protein, mouseGdf15 protein, mouseGrowth Differentiation Factor 15

Identifiers

PMID21455723
PMCPMC3105238
OpenAlexW1976521356

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.