Evidence map›Paper›PMID 26996756›Full record

ReviewJournal of molecular and cellular cardiology2016

Myocyte-fibroblast communication in cardiac fibrosis and arrhythmias: Mechanisms and model systems.

Jason Pellman, Jing Zhang, Farah Sheikh

Abstract readReview
In one paragraph

Review in Journal of molecular and cellular cardiology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 108 papers.

0numbers the graph read from it
0cells of the map it votes in
108citing papers in PubMed
9.6field-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

108 citing papers in PubMed, 162 citations in OpenAlex.

  1. Article
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  4. Article
  5. Review
  6. Review
  7. Article
  8. Article
  9. Article
  10. Advances in RNA modification in myocardial fibrosis (Review).International journal of molecular medicine · 2025
    Review
  11. Article
  12. Review
  13. Review
  14. Article
  15. Review
  16. Article
  17. Dressed in Collagen: 2D and 3D Cardiac Fibrosis Models.International journal of molecular sciences · 2025
    Review
  18. Review
  19. Short-Term Electrical Stimulation Impacts Cardiac Cell Structure and Function.Journal of tissue engineering and regenerative medicine · 2025
    Article
  20. Article

48 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

3 authors at 1 institution in 1 country.

Jason PellmanDepartment of Medicine, University of California-San Diego, 9500 Gilman Drive, La Jolla, CA 92093, USA.
Jing ZhangDepartment of Medicine, University of California-San Diego, 9500 Gilman Drive, La Jolla, CA 92093, USA.
Farah SheikhDepartment of Medicine, University of California-San Diego, 9500 Gilman Drive, La Jolla, CA 92093, USA. Electronic address: fasheikh@ucsd.edu.
University of California, San Diego · US

Funding

The molecular mechanisms underlying arrhythmogenic right ventricular dysplasia/cardiomyopathyR01HL095780 · NHLBI · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI SHEIKH, FARAH · 2009 to 2018
$3.9M
The Role of SNAP29, a Novel Desmoplakin Interactor, in Cardiac PathophysiologyF31HL120611 · NHLBI · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI PELLMAN, JASON R · 2013 to 2015
$72k
ANALYSIS OF AX1 RECEPTOR SIGNAL TRANSDUCTIONF32HL009780 · NHLBI · UNIVERSITY OF WASHINGTON · PI MELARAGNO, MATTHEW G · 1997 to 1999
–
NHLBI NIH HHS F31 HL120611NHLBI NIH HHS F32 HL009780NHLBI NIH HHS R01 HL095780
6 · The paper itself

Abstract

Development of cardiac fibrosis and arrhythmias is controlled by the activity of and communication between cardiomyocytes and fibroblasts in the heart. Myocyte-fibroblast interactions occur via both direct and indirect means including paracrine mediators, extracellular matrix interactions, electrical modulators, mechanical junctions, and membrane nanotubes. In the diseased heart, cardiomyocyte and fibroblast ratios and activity, and thus myocyte-fibroblast interactions, change and are thought to contribute to the course of disease including development of fibrosis and arrhythmogenic activity. Fibroblasts have a developing role in modulating cardiomyocyte electrical and hypertrophic activity, however gaps in knowledge regarding these interactions still exist. Research in this field has necessitated the development of unique approaches to isolate and control myocyte-fibroblast interactions. Numerous methods for 2D and 3D co-culture systems have been developed, while a growing part of this field is in the use of better tools for in vivo systems including cardiomyocyte and fibroblast specific Cre mouse lines for cell type specific genetic ablation. This review will focus on (i) mechanisms of myocyte-fibroblast communication and their effects on disease features such as cardiac fibrosis and arrhythmias as well as (ii) methods being used and currently developed in this field.

Indexed as

Cell CommunicationAnimalsArrhythmias, CardiacCoculture TechniquesDisease Models, AnimalExtracellular MatrixExtracellular Matrix ProteinsFibroblastsFibrosisHumansIn Vitro TechniquesModels, BiologicalMyocardiumMyocytes, CardiacExtracellular Matrix ProteinsArrhythmiaCardiomyocyteCell-cell interactionsFibroblastFibrosis

Identifiers

PMID26996756
PMCPMC4861678
OpenAlexW2301176136

What OpenQuestion holds

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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.