Evidence map›Paper›PMID 27234440›Full record

ArticleEMBO molecular medicine2016

Follistatin-like 1 promotes cardiac fibroblast activation and protects the heart from rupture.

Sonomi Maruyama, Kazuto Nakamura, Kyriakos N Papanicolaou, Soichi Sano, Ippei Shimizu, Yasuhide Asaumi, Maurice J van den Hoff, Noriyuki Ouchi, Fabio A Recchia, Kenneth Walsh

Open access · goldAbstract read
In one paragraph

Article in EMBO molecular medicine, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 71 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
71citing papers in PubMed, 1 pooled it
8.8field-weighted citation impact, top 2% 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

71 citing papers in PubMed, 1 synthesis or guideline pooled it, 109 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Signaling pathways regulating cardiac regeneration.Cell regeneration (London, England) · 2026
    Review
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11 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

10 authors at 4 institutions in 4 countries.

Sonomi MaruyamaDepartment of Molecular Cardiology, Whitaker Cardiovascular Institute, Boston University School of Medicine, Boston, MA, USA.
Kazuto NakamuraDepartment of Molecular Cardiology, Whitaker Cardiovascular Institute, Boston University School of Medicine, Boston, MA, USA.
Kyriakos N PapanicolaouDepartment of Molecular Cardiology, Whitaker Cardiovascular Institute, Boston University School of Medicine, Boston, MA, USA.
Soichi SanoDepartment of Molecular Cardiology, Whitaker Cardiovascular Institute, Boston University School of Medicine, Boston, MA, USA.
Ippei ShimizuDepartment of Molecular Cardiology, Whitaker Cardiovascular Institute, Boston University School of Medicine, Boston, MA, USA.
Yasuhide AsaumiDepartment of Molecular Cardiology, Whitaker Cardiovascular Institute, Boston University School of Medicine, Boston, MA, USA.
Maurice J van den HoffDepartment of Anatomy, Embryology and Physiology, Academic Medical Center, Amsterdam, The Netherlands.
Noriyuki OuchiMolecular Cardiovascular Medicine, Nagoya University Graduate School of Medicine, Showa-ku, Nagoya, Japan.
Fabio A RecchiaCardiovascular Research Center, Lewis Katz School of Medicine at Temple University, Philadelphia, PA, USA Institute of Life Sciences, Scuola Superiore Sant'Anna, Pisa, Italy.
Kenneth WalshDepartment of Molecular Cardiology, Whitaker Cardiovascular Institute, Boston University School of Medicine, Boston, MA, USA kxwalsh@bu.edu.ORCID 0000-0001-7580-2276
Boston University · USAmsterdam UMC Location University of Amsterdam · NLNagoya University · JPScuola Superiore Sant'Anna · IT

Funding

Redox regulation in Endothelial Progenitor CellsP01HL081587 · NHLBI · BOSTON UNIVERSITY MEDICAL CAMPUS · PI WALSH, KENNETH · 2005 to 2015
$21.5M
Substrate Selection and Oxidative Stress in Heart FailureP01HL074237 · NHLBI · UNIVERSITY OF MARYLAND BALTIMORE · PI STANLEY, WILLIAM C · 2003 to 2013
$19.9M
Anti-Angiogenic Mechanisms in Human ObesityR01HL126141 · NHLBI · BOSTON UNIVERSITY MEDICAL CAMPUS · PI GOKCE, NOYAN, WALSH, KENNETH · 2015 to 2019
$2.4M
Inflammatory Wnt signaling in ischemic myocardiumR01HL131006 · NHLBI · UNIVERSITY OF VIRGINIA · PI WALSH, KENNETH · 2016 to 2019
$2.1M
VEGF receptor-1-mediated protection in dilated cardiomyopathyR01HL108213 · NHLBI · TEMPLE UNIV OF THE COMMONWEALTH · PI RECCHIA, FABIO A · 2012 to 2015
$1.6M
Mitochondrial dynamics and cardiac remodelingR01HL120160 · NHLBI · BOSTON UNIVERSITY MEDICAL CAMPUS · PI WALSH, KENNETH · 2013 to 2016
$1.6M
Paracrine Regulation of Heart FailureR01HL116591 · NHLBI · BOSTON UNIVERSITY MEDICAL CAMPUS · PI WALSH, KENNETH · 2013 to 2016
$1.6M
Myokine Control of Hepatic SteatosisR21AG052160 · NIA · BOSTON UNIVERSITY MEDICAL CAMPUS · PI WALSH, KENNETH · 2016 to 2017
$452k
NHLBI NIH HHS P01 HL074237NHLBI NIH HHS P01 HL081587NHLBI NIH HHS R01 HL108213NHLBI NIH HHS R01 HL116591NHLBI NIH HHS R01 HL120160NHLBI NIH HHS R01 HL126141NHLBI NIH HHS R01 HL131006NIA NIH HHS R21 AG052160
6 · The paper itself

Abstract

Follistatin-like 1 (Fstl1) is a secreted protein that is acutely induced in heart following myocardial infarction (MI). In this study, we investigated cell type-specific regulation of Fstl1 and its function in a murine model of MI Fstl1 was robustly expressed in fibroblasts and myofibroblasts in the infarcted area compared to cardiac myocytes. The conditional ablation of Fstl1 in S100a4-expressing fibroblast lineage cells (Fstl1-cfKO mice) led to a reduction in injury-induced Fstl1 expression and increased mortality due to cardiac rupture during the acute phase. Cardiac rupture was associated with a diminished number of myofibroblasts and decreased expression of extracellular matrix proteins. The infarcts of Fstl1-cfKO mice displayed weaker birefringence, indicative of thin and loosely packed collagen. Mechanistically, the migratory and proliferative capabilities of cardiac fibroblasts were attenuated by endogenous Fstl1 ablation. The activation of cardiac fibroblasts by Fstl1 was mediated by ERK1/2 but not Smad2/3 signaling. This study reveals that Fstl1 is essential for the acute repair of the infarcted myocardium and that stimulation of early fibroblast activation is a novel function of Fstl1.

Indexed as

AnimalsDisease Models, AnimalEndopeptidasesFibroblast Activation Protein AlphaFibroblastsFollistatinFollistatin-Related ProteinsGelatinasesMembrane ProteinsMiceMice, KnockoutMyocardial InfarctionRuptureSerine EndopeptidasesSurvival AnalysisEndopeptidasesFibroblast Activation Protein AlphaFollistatinFollistatin-Related ProteinsGelatinasesMembrane ProteinsSerine Endopeptidasescardiokinefibrosisinfarct healingmyocardial infarction

Identifiers

PMID27234440
PMCPMC4967946
OpenAlexW2401757307

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.