Evidence map›Paper›PMID 24005378›Full record

ReviewJournal of muscle research and cell motility2013

Alpha-tropomyosin mutations in inherited cardiomyopathies.

Charles Redwood, Paul Robinson

Open access · greenAbstract readReview
PubMed Publisher
In one paragraph

Review in Journal of muscle research and cell motility, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 61 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
61citing papers in PubMed, 1 pooled it
3.6field-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

61 citing papers in PubMed, 1 synthesis or guideline pooled it, 92 citations in OpenAlex.

  1. Role of miRNA in Cardiovascular Diseases in Children-Systematic Review.International journal of molecular sciences · 2024
    Pooled it
  2. Article
  3. Review
  4. Review
  5. Article
  6. Evaluating Pathogenicity ofJournal of precision medicine (Amsterdam, Netherlands) · 2025
    Article
  7. Article
  8. Article
  9. Frontiers in genetics · 2025
    Article
  10. Case report: cosegregation of a TPM1 in-frame deletion (p.Lys7del) with familial non-compaction cardiomyopathy (NCCM).Clinical research in cardiology : official journal of the German Cardiac Society · 2024
    Article
  11. Article
  12. A NovelIndian journal of clinical biochemistry : IJCB · 2024
    Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Review
  19. Genetic predisposition study of heart failure and its association with cardiomyopathy.The Egyptian heart journal : (EHJ) : official bulletin of the Egyptian Society of Cardiology · 2022
    Review
  20. Review

1 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

2 authors at 1 institution in 1 country.

Charles RedwoodDivision of Cardiovascular Medicine, Radcliffe Department of Medicine, John Radcliffe Hospital, University of Oxford, West Wing Level 6, Oxford, OX3 9DU, UK, credwood@well.ox.ac.uk.
Paul Robinson
University of Oxford · GB

Funding

British Heart Foundation
6 · The paper itself

Abstract

The inherited cardiac diseases hypertrophic cardiomyopathy (HCM) and dilated cardiomyopathy (DCM) can both be caused by missense mutations in the TPM1 gene which encodes the thin filament regulatory protein α-tropomyosin. Different mutations are responsible for either HCM or DCM, suggesting that distinct changes in tropomyosin structure and function can lead to the different diseases. Various biophysical and physiological approaches have been used to investigate the structure-function effects of the mutations, and animal models developed. The reported effects of the mutations include changes to the secondary structure of tropomyosin, its binding to actin and its position on the thin filament, and alterations to actin-myosin interactions and myofilament Ca(2+) sensitivity. The latter changes have been found to be particularly consistent, with HCM mutations increasing Ca(2+) sensitivity and DCM mutations in general decreasing this parameter and uncoupling the effect of troponin phosphorylation upon Ca(2+) responsiveness. As well as impacting on contractility, these changes are likely to alter intracellular Ca(2+) handling and signaling, and a combination of these alterations may provide the trigger for disease remodeling.

Indexed as

Mutation, MissenseAnimalsCardiomyopathy, DilatedCardiomyopathy, Hypertrophic, FamilialDisease Models, AnimalHumansTropomyosinTropomyosin

Identifiers

PMID24005378
OpenAlexW2058118262

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.