Evidence map›Paper›PMID 37834293›Full record

ReviewInternational journal of molecular sciences2023

Myocardial Fibrosis in Hypertrophic Cardiomyopathy: A Perspective from Fibroblasts.

Maja Schlittler, Peter P Pramstaller, Alessandra Rossini, Marzia De Bortoli

Open access · goldAbstract readReview
In one paragraph

Review in International journal of molecular sciences, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
46citing papers in PubMed, 1 pooled it
10.3field-weighted citation impact, top 1% 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

46 citing papers in PubMed, 1 synthesis or guideline pooled it, 47 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Article
  4. Article
  5. Review
  6. Article
  7. Article
  8. Fragmented QRS complex in athletes' electrocardiogram: physiological adaptation or pathological sign? A scoping review.The Egyptian heart journal : (EHJ) : official bulletin of the Egyptian Society of Cardiology · 2026
    Review
  9. Article
  10. Optimization of the in vitro Model of Cardiac Fibrosis.Brazilian journal of cardiovascular surgery · 2026
    Article
  11. Article
  12. Review
  13. Article
  14. Article
  15. Review
  16. Article
  17. Article
  18. Article
  19. Clinical Outcomes Post-Transcatheter Aortic Valve Replacement in Patients With Hypertrophic Obstructive Cardiomyopathy.Catheterization and cardiovascular interventions : official journal of the Society for Cardiac Angiography & Interventions · 2025
    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 1 country.

Maja SchlittlerEurac Research, Institute for Biomedicine (Affiliated to the University of Lübeck), 39100 Bolzano, Italy.ORCID 0000-0002-3886-9612
Peter P PramstallerEurac Research, Institute for Biomedicine (Affiliated to the University of Lübeck), 39100 Bolzano, Italy.
Alessandra RossiniEurac Research, Institute for Biomedicine (Affiliated to the University of Lübeck), 39100 Bolzano, Italy.ORCID 0000-0002-0440-1130
Marzia De BortoliEurac Research, Institute for Biomedicine (Affiliated to the University of Lübeck), 39100 Bolzano, Italy.ORCID 0000-0002-1348-1304
Eurac Research · IT

Funding

The Autonomous Province of Bolzano/ Bozen South Tyrol in the framework of the Programme "International Mobility of Researchers 18021/2020"
6 · The paper itself

Abstract

Hypertrophic cardiomyopathy (HCM) is the most common inherited heart disease and the leading cause of sudden cardiac death in young people. Mutations in genes that encode structural proteins of the cardiac sarcomere are the more frequent genetic cause of HCM. The disease is characterized by cardiomyocyte hypertrophy and myocardial fibrosis, which is defined as the excessive deposition of extracellular matrix proteins, mainly collagen I and III, in the myocardium. The development of fibrotic tissue in the heart adversely affects cardiac function. In this review, we discuss the latest evidence on how cardiac fibrosis is promoted, the role of cardiac fibroblasts, their interaction with cardiomyocytes, and their activation via the TGF-β pathway, the primary intracellular signalling pathway regulating extracellular matrix turnover. Finally, we summarize new findings on profibrotic genes as well as genetic and non-genetic factors involved in the pathophysiology of HCM.

Indexed as

Cardiomyopathy, HypertrophicAdolescentFibroblastsFibrosisHumansMyocardiumMyocytes, Cardiaccardiac fibroblasthypertrophic cardiomyopathymyocardial fibrosismyofibroblastsTGF-β

Identifiers

PMID37834293
PMCPMC10573356
OpenAlexW4387267527

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.