Evidence map›Paper›PMID 11972068›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2002

Dilated cardiomyopathy in mice deficient for the lysosomal cysteine peptidase cathepsin L.

Jörg Stypmann, Kerstin Gläser, Wera Roth, Desmond J Tobin, Ivonne Petermann, Rainer Matthias, Gerold Mönnig, Wilhelm Haverkamp, Günter Breithardt, Wolfgang Schmahl and 2 more

Open access · greenAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 63 papers.

0numbers the graph read from it
0cells of the map it votes in
63citing papers in PubMed
4.3field-weighted citation impact, top 5% 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

63 citing papers in PubMed, 180 citations in OpenAlex.

  1. Trial
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  5. Review
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  7. Article
  8. Insights from the use of erythropoietin in experimental Chagas disease.International journal for parasitology. Drugs and drug resistance · 2022
    Article
  9. Article
  10. Article
  11. Article
  12. Pathogenesis and Management of COVID-19.Journal of xenobiotics · 2021
    Review
  13. Article
  14. Cysteinyl cathepsins in cardiovascular diseases.Biochimica et biophysica acta. Proteins and proteomics · 2020
    Review
  15. Review
  16. Article
  17. Review
  18. Mast cell-deficiency protects mice from streptozotocin-induced diabetic cardiomyopathy.Translational research : the journal of laboratory and clinical medicine · 2019
    Article
  19. Review
  20. Article

3 more citing papers are in PubMed but not listed here.

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

12 authors at 2 institutions in 2 countries.

Jörg StypmannMedizinische Klinik und Poliklinik C (Kardiologie und Angiologie), Universitätsklinikum Westfälische Wilhelms-Universität Münster, D-48149 Münster, Germany.
Kerstin Gläser
Wera Roth
Desmond J Tobin
Ivonne Petermann
Rainer Matthias
Gerold Mönnig
Wilhelm Haverkamp
Günter Breithardt
Wolfgang Schmahl
Christoph Peters
Thomas Reinheckel
Saint Louis University · USUniversity of Bradford · GB

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Dilated cardiomyopathy is a frequent cause of heart failure and is associated with high mortality. Progressive remodeling of the myocardium leads to increased dimensions of heart chambers. The role of intracellular proteolysis in the progressive remodeling that underlies dilated cardiomyopathy has not received much attention yet. Here, we report that the lysosomal cysteine peptidase cathepsin L (CTSL) is critical for cardiac morphology and function. One-year-old CTSL-deficient mice show significant ventricular and atrial enlargement that is associated with a comparatively small increase in relative heart weight. Interstitial fibrosis and pleomorphic nuclei were found in the myocardium of the knockout mice. By electron microscopy, CTSL-deficient cardiomyocytes contained multiple large and apparently fused lysosomes characterized by storage of electron-dense heterogeneous material. Accordingly, the assessment of left ventricular function by echocardiography revealed severely impaired myocardial contraction in the CTSL-deficient mice. In addition, echocardiographic and electrocardiographic findings to some degree point to left ventricular hypertrophy that most likely represents an adaptive response to cardiac impairment. The histomorphological and functional alterations of CTSL-deficient hearts result in valve insufficiencies. Furthermore, abnormal heart rhythms, like supraventricular tachycardia, ventricular extrasystoles, and first-degree atrioventricular block, were detected in the CTSL-deficient mice.

Indexed as

AnimalsCardiomyopathy, DilatedCathepsin LCathepsinsCysteine EndopeptidasesEchocardiographyElectrocardiographyFemaleHeart ValvesLysosomesMaleMiceMicroscopy, ElectronOrgan SizeTime FactorsCathepsin LCathepsinsCtsl protein, mouseCysteine Endopeptidases

Identifiers

PMID11972068
PMCPMC122932
OpenAlexW2043476842

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.