Evidence map›Paper›PMID 22898751›Full record

ReviewJournal of cardiovascular translational research2012

The actin-MRTF-SRF gene regulatory axis and myofibroblast differentiation.

Eric M Small

Abstract readReview
PubMed Publisher
In one paragraph

Review in Journal of cardiovascular translational research, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 90 papers.

0numbers the graph read from it
0cells of the map it votes in
90citing papers in PubMed
4.6field-weighted citation impact, top 5% 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

90 citing papers in PubMed, 146 citations in OpenAlex.

  1. Article
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  9. Inhibition of the MRTF-A/SRF signaling axis alleviates vocal fold scarring.Matrix biology : journal of the International Society for Matrix Biology · 2025
    Article
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30 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

1 author at 1 institution in 1 country.

Eric M SmallAab Cardiovascular Research Institute, Department of Medicine, School of Medicine and Dentistry, University of Rochester, 601 Elmwood Avenue, Box CVRI, Rochester, NY 14642, USA. Eric_Small@URMC.Rochester.edu
University of Rochester · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cardiac fibroblasts are responsible for necrotic tissue replacement and scar formation after myocardial infarction (MI) and contribute to remodeling in response to pathological stimuli. This response to insult or injury is largely due to the phenotypic plasticity of fibroblasts. When fibroblasts encounter environmental disturbances, whether biomechanical or humoral, they often transform into smooth muscle-like, contractile cells called "myofibroblasts." The signals that control myofibroblast differentiation include the transforming growth factor (TGF)-β1-Smad pathway and Rho GTPase-dependent actin polymerization. Recent evidence implicates serum response factor (SRF) and the myocardin-related transcription factors (MRTFs) as key mediators of the contractile gene program in response to TGF-β1 or RhoA signaling. This review highlights the function of myofibroblasts in cardiac remodeling and the role of the actin-MRTF-SRF signaling axis in regulating this process.

Indexed as

Cell DifferentiationActinsAnimalsFibrosisGene Expression RegulationHeart DiseasesHumansMyocardiumMyofibroblastsPhenotypeSerum Response FactorSignal TransductionTranscription FactorsActinsSerum Response FactorTranscription Factors

Identifiers

PMID22898751
OpenAlexW2061676790

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.