Evidence map›Paper›PMID 23440276›Full record

ArticleThe Journal of general physiology2013

Knockdown of desmin in zebrafish larvae affects interfilament spacing and mechanical properties of skeletal muscle.

Mei Li, Monika Andersson-Lendahl, Thomas Sejersen, Anders Arner

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of general physiology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
3.4field-weighted citation impact, top 7% 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

26 citing papers in PubMed, 56 citations in OpenAlex.

  1. Review
  2. Article
  3. Molecular Pathways and Animal Models of Cardiomyopathies.Advances in experimental medicine and biology · 2024
    Article
  4. Review
  5. Review
  6. Article
  7. Article
  8. Article
  9. Generation of desminopathy in rats using CRISPR-Cas9.Journal of cachexia, sarcopenia and muscle · 2020
    Article
  10. Chronic exposure to copper oxide nanoparticles causes muscle toxicity in adult zebrafish.Environmental science and pollution research international · 2020
    Article
  11. Effect of Ataluren on dystrophin mutations.Journal of cellular and molecular medicine · 2020
    Article
  12. Zebrafish models of sarcopenia.Disease models & mechanisms · 2020
    Review
  13. Article
  14. Article
  15. Review
  16. Review
  17. Review
  18. Disruption of Nuclear Receptor Signaling Alters Triphenyl Phosphate-Induced Cardiotoxicity in Zebrafish Embryos.Toxicological sciences : an official journal of the Society of Toxicology · 2018
    Article
  19. Article
  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

4 authors at 1 institution in 2 countries.

Mei LiDepartment of Physiology and Pharmacology, Karolinska Institutet, SE 171 77 Stockholm, Sweden.
Monika Andersson-Lendahl
Thomas Sejersen
Anders Arner
Karolinska Institutet · SE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Skeletal muscle was examined in zebrafish larvae in order to address questions related to the function of the intermediate filament protein desmin and its role in the pathogenesis of human desminopathy. A novel approach including mechanical and structural studies of 4-6-d-old larvae was applied. Morpholino antisense oligonucleotides were used to knock down desmin. Expression was assessed using messenger RNA and protein analyses. Histology and synchrotron light-based small angle x-ray diffraction were applied. Functional properties were analyzed with in vivo studies of swimming behavior and with in vitro mechanical examinations of muscle. The two desmin genes normally expressed in zebrafish could be knocked down by ~50%. This resulted in a phenotype with disorganized muscles with altered attachments to the myosepta. The knockdown larvae were smaller and had diminished swimming activity. Active tension was lowered and muscles were less vulnerable to acute stretch-induced injury. X-ray diffraction revealed wider interfilament spacing. In conclusion, desmin intermediate filaments are required for normal active force generation and affect vulnerability during eccentric work. This is related to the role of desmin in anchoring sarcomeres for optimal force transmission. The results also show that a partial lack of desmin, without protein aggregates, is sufficient to cause muscle pathology resembling that in human desminopathy.

Indexed as

AnimalsDesminGene Knockdown TechniquesIntermediate Filament ProteinsIntermediate FilamentsLarvaMuscle ContractionMuscle, SkeletalPhenotypeSarcomeresStress, MechanicalSwimmingX-Ray DiffractionZebrafishDesminIntermediate Filament Proteins

Identifiers

PMID23440276
PMCPMC3581687
OpenAlexW2144623006

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-SA
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.