Evidence map›Paper›PMID 24189039›Full record

ReviewJournal of molecular and cellular cardiology2014

Myofibroblasts: trust your heart and let fate decide.

Jennifer Davis, Jeffery D Molkentin

Open access · greenAbstract readReview
In one paragraph

Review in Journal of molecular and cellular cardiology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 215 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
215citing papers in PubMed, 2 pooled it
15.8field-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

215 citing papers in PubMed, 2 syntheses or guidelines pooled it, 353 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Article
  4. Article
  5. [A new method for extracting adult mouse cardiac fibroblasts more efficiently and stably].Beijing da xue xue bao. Yi xue ban = Journal of Peking University. Health sciences · 2026
    Article
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  10. Review
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  16. Tailored therapeutics for cardiomyopathies.Nature reviews. Cardiology · 2025
    Review
  17. Article
  18. Advances in fibroblast-based cardiac reprogramming in the treatment of heart disease.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2025
    Review
  19. Article
  20. Review

155 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 2 institutions in 1 country.

Jennifer DavisDepartment of Pediatrics, University of Cincinnati, Cincinnati Children's Hospital Medical Center, Cincinnati, OH 45229, USA.
Jeffery D MolkentinDepartment of Pediatrics, University of Cincinnati, Cincinnati Children's Hospital Medical Center, Cincinnati, OH 45229, USA; Howard Hughes Medical Institute, Cincinnati, OH 45229, USA. Electronic address: jeff.molkentin@cchmc.org.
Cincinnati Children's Hospital Medical Center · USUniversity of Cincinnati · US

Funding

WNT/^-catenin Signaling and Cardiac Fibrosis P01HL069779 · NHLBI · CINCINNATI CHILDRENS HOSP MED CTR · PI MOLKENTIN, JEFFERY D · 2002 to 2017
$27.0M
PKC alpha as a translational target in Heart FailureP01HL108806 · NHLBI · TEMPLE UNIV OF THE COMMONWEALTH · PI RABINOWITZ, JOSEPH E · 2012 to 2016
$11.3M
Thrombospondin 4 regulates adaptive ER stress responseRenewal - Resubmission - 1R01HL105924 · NHLBI · CINCINNATI CHILDRENS HOSP MED CTR · PI Jeffery D Molkentin · 2011 to 2026
$7.3M
Regulation of TGF - (beta) pathways in muscular dystrophy fibrosisP01NS072027 · NINDS · UNIVERSITY OF CHICAGO · PI MCNALLY, ELIZABETH M · 2011 to 2015
$6.2M
Molecular Pathways Controlling Cardiac Gene ExpressionR37HL060562 · NHLBI · CINCINNATI CHILDRENS HOSP MED CTR · PI MOLKENTIN, JEFFERY D · 2008 to 2017
$3.8M
MBNL1's function in myofibroblast transformation and fibrosisR00HL119353 · NHLBI · UNIVERSITY OF WASHINGTON · PI DAVIS, JENNIFER MICHELLE · 2015 to 2017
$747k
MBNL1's function in myofibroblast transformation and fibrosisK99HL119353 · NHLBI · CINCINNATI CHILDRENS HOSP MED CTR · PI DAVIS, JENNIFER MICHELLE · 2013 to 2014
$262k
NHLBI NIH HHS K99 HL119353NHLBI NIH HHS P01 HL069779NHLBI NIH HHS P01 HL108806NHLBI NIH HHS R00 HL119353NHLBI NIH HHS R01 HL105924NHLBI NIH HHS R37 HL060562NINDS NIH HHS P01 NS072027
6 · The paper itself

Abstract

Cardiac fibrosis is a substantial problem in managing multiple forms of heart disease. Fibrosis results from an unrestrained tissue repair process orchestrated predominantly by the myofibroblast. These are highly specialized cells characterized by their ability to secrete extracellular matrix (ECM) components and remodel tissue due to their contractile properties. This contractile activity of the myofibroblast is ascribed, in part, to the expression of smooth muscle α-actin (αSMA) and other tension-associated structural genes. Myofibroblasts are a newly generated cell type derived largely from residing mesenchymal cells in response to both mechanical and neurohumoral stimuli. Several cytokines, chemokines, and growth factors are induced in the injured heart, and in conjunction with elevated wall tension, specific signaling pathways and downstream effectors are mobilized to initiate myofibroblast differentiation. Here we will review the cell fates that contribute to the myofibroblast as well as nodal molecular signaling effectors that promote their differentiation and activity. We will discuss canonical versus non-canonical transforming growth factor-β (TGFβ), angiotensin II (AngII), endothelin-1 (ET-1), serum response factor (SRF), transient receptor potential (TRP) channels, mitogen-activated protein kinases (MAPKs) and mechanical signaling pathways that are required for myofibroblast transformation and fibrotic disease. This article is part of a Special Issue entitled "Myocyte-Fibroblast Signalling in Myocardium ".

Indexed as

Mechanotransduction, CellularMyofibroblastsActinsAngiotensin IICell DifferentiationEndothelin-1Extracellular MatrixFibrosisGene Expression RegulationHeartHumansMitogen-Activated Protein KinasesSerum Response FactorTransforming Growth Factor betaACTA2 protein, humanActinsAngiotensin IIEndothelin-1Mitogen-Activated Protein KinasesSerum Response FactorTransforming Growth Factor betaAngiotensin IIExtracellular matrixFibrosisSerum response factorTGFβTRP channel

Identifiers

PMID24189039
PMCPMC3995855
OpenAlexW2066885817

What OpenQuestion holds

Textmetadata
LicenceTDM
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.