Evidence map›Paper›PMID 34445638›Full record

ReviewInternational journal of molecular sciences2021

Pathogenic Mechanisms of Hypertrophic Cardiomyopathy beyond Sarcomere Dysfunction.

Chun Chou, Michael T Chin

Open access · goldAbstract readReview
In one paragraph

Review in International journal of molecular sciences, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed
4.6field-weighted citation impact, top 4% 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

33 citing papers in PubMed, 40 citations in OpenAlex.

  1. Review
  2. Review
  3. Review
  4. Article
  5. Article
  6. Spectrum and Clinical Interpretation ofInternational journal of molecular sciences · 2025
    Article
  7. Review
  8. Review
  9. Hypertrophic Cardiomyopathy-Associated CRYABInternational journal of molecular sciences · 2025
    Article
  10. Review
  11. The E2F family: a ray of dawn in cardiomyopathy.Molecular and cellular biochemistry · 2025
    Review
  12. Article
  13. Single Cell Transcriptomic Profiling ofJournal of the American Heart Association · 2025
    Article
  14. Article
  15. Review
  16. Article
  17. Review
  18. Article
  19. Review
  20. Review
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.

Chun ChouDepartment of Medicine, Tufts University School of Medicine, Boston, MA 02111, USA.
Michael T ChinDepartment of Medicine, Tufts University School of Medicine, Boston, MA 02111, USA.ORCID 0000-0003-3065-8498
Tufts University · US

Funding

Tufts Clinical and Translational Science Institute (Pilot Supplement)UL1TR002544 · NCATS · TUFTS UNIVERSITY BOSTON · PI SELKER, HARRY P. · 2018 to 2022
$50.2M
American Heart Association 18IPA34170294NCATS NIH HHS UL1TR002544
6 · The paper itself

Abstract

Hypertrophic cardiomyopathy (HCM) is the most common inherited cardiovascular disorder, affecting 1 in 500 people in the general population. Although characterized by asymmetric left ventricular hypertrophy, cardiomyocyte disarray, and cardiac fibrosis, HCM is in fact a highly complex disease with heterogenous clinical presentation, onset, and complications. While HCM is generally accepted as a disease of the sarcomere, variable penetrance in families with identical genetic mutations challenges the monogenic origin of HCM and instead implies a multifactorial cause. Furthermore, large-scale genome sequencing studies revealed that many genes previously reported as causative of HCM in fact have little or no evidence of disease association. These findings thus call for a re-evaluation of the sarcomere-centered view of HCM pathogenesis. Here, we summarize our current understanding of sarcomere-independent mechanisms of cardiomyocyte hypertrophy, highlight the role of extracellular signals in cardiac fibrosis, and propose an alternative but integrated model of HCM pathogenesis.

Indexed as

Genetic Predisposition to DiseasePhenotypeCardiomyopathy, HypertrophicHumansSarcomerescardiac fibroblastcardiac fibrosiscardiac myocyteextracellular matrixhypertrophic cardiomyopathymyocyte–fibroblast interactionpathological cardiac hypertrophysarcomere

Identifiers

PMID34445638
PMCPMC8396307
OpenAlexW3182544947

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.