Evidence map›Paper›PMID 24650916›Full record

ArticleCirculation research2014

Cardiogenic genes expressed in cardiac fibroblasts contribute to heart development and repair.

Milena B Furtado, Mauro W Costa, Edward A Pranoto, Ekaterina Salimova, Alexander R Pinto, Nicholas T Lam, Anthony Park, Paige Snider, Anjana Chandran, Richard P Harvey and 5 more

Open access · bronzeAbstract read
In one paragraph

Article in Circulation research, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 144 papers.

0numbers the graph read from it
0cells of the map it votes in
144citing papers in PubMed
10.2field-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

144 citing papers in PubMed, 216 citations in OpenAlex.

  1. Article
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  9. Frontiers in cell and developmental biology · 2026
    Article
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  11. Article
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  13. Article
  14. Region- and Cell-type-Resolved Multiomic Atlas of the Heart.Molecular & cellular proteomics : MCP · 2025
    Article
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  17. Review
  18. Review
  19. Article
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84 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

15 authors at 3 institutions in 2 countries.

Milena B FurtadoFrom the Australian Regenerative Medicine Institute (M.B.F., M.W.C., E.A.P., E.S., A.R.P., A.C., N.A.R.), Department of Anatomy and Developmental Biology (A.R.P., R.B.), and Monash Biomedical Imaging (J.P.), Monash University, Melbourne, Victoria, Australia; Baker IDI Heart and Diabetes Institute, Melbourne, Victoria, Australia (N.T.L., D.M.K.); Department of Pediatrics, Indiana University School of Medicine, Indianapolis (P.S., S.J.C.); and Victor Chang Cardiac Research Institute, Darlinghurst, New South Wales, Australia (R.P.H.).
Mauro W Costa
Edward A Pranoto
Ekaterina Salimova
Alexander R Pinto
Nicholas T Lam
Anthony Park
Paige Snider
Anjana Chandran
Richard P Harvey
Richard Boyd
Simon J Conway
James Pearson
David M Kaye
Nadia A Rosenthal
Indiana University – Purdue University Indianapolis · USIndiana University School of MedicineBaker Heart and Diabetes Institute · AU

Funding

NEURAL-CREST RELATED HEART DEFECTSR01HL060714 · NHLBI · MEDICAL COLLEGE OF GEORGIA (MCG) · PI CONWAY, SIMON JAMES · 1998 to 2017
$4.7M
NHLBI NIH HHS R01 HL060714
6 · The paper itself

Abstract

rationaleCardiac fibroblasts are critical to proper heart function through multiple interactions with the myocardial compartment, but appreciation of their contribution has suffered from incomplete characterization and lack of cell-specific markers.

objectiveTo generate an unbiased comparative gene expression profile of the cardiac fibroblast pool, identify and characterize the role of key genes in cardiac fibroblast function, and determine their contribution to myocardial development and regeneration. METHODS AND

resultsHigh-throughput cell surface and intracellular profiling of cardiac and tail fibroblasts identified canonical mesenchymal stem cell and a surprising number of cardiogenic genes, some expressed at higher levels than in whole heart. While genetically marked fibroblasts contributed heterogeneously to interstitial but not cardiomyocyte compartments in infarcted hearts, fibroblast-restricted depletion of one highly expressed cardiogenic marker, T-box 20, caused marked myocardial dysmorphology and perturbations in scar formation on myocardial infarction.

conclusionsThe surprising transcriptional identity of cardiac fibroblasts, the adoption of cardiogenic gene programs, and direct contribution to cardiac development and repair provoke alternative interpretations for studies on more specialized cardiac progenitors, offering a novel perspective for reinterpreting cardiac regenerative therapies.

Indexed as

Gene Expression Regulation, DevelopmentalAnimalsBiomarkersCells, CulturedDisease Models, AnimalFibroblastsGene Expression ProfilingGene Regulatory NetworksGreen Fluorescent ProteinsHigh-Throughput Nucleotide SequencingHumansMaleMesenchymal Stem CellsMiceMice, Inbred C57BLMice, KnockoutBiomarkersGreen Fluorescent ProteinsGt(ROSA)26Sor non-coding RNA, mouseRNA, UntranslatedT-Box Domain ProteinsTbx20 protein, mousecardiac fibroblastsgene regulatory networkshearttranscription factors

Identifiers

PMID24650916
PMCPMC4083003
OpenAlexW2129660202

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.