Evidence map›Paper›PMID 21505261›Full record

ArticleThe Journal of clinical investigation2011

Adult mouse epicardium modulates myocardial injury by secreting paracrine factors.

Bin Zhou, Leah B Honor, Huamei He, Qing Ma, Jin-Hee Oh, Catherine Butterfield, Ruei-Zeng Lin, Juan M Melero-Martin, Elena Dolmatova, Heather S Duffy and 10 more

Open access · greenAbstract read
In one paragraph

Article in The Journal of clinical investigation, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 338 papers.

0numbers the graph read from it
0cells of the map it votes in
338citing papers in PubMed
16.2field-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

338 citing papers in PubMed, 514 citations in OpenAlex.

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  19. Heart-derived endogenous stem cells.Molecular biology reports · 2025
    Review
  20. Article

278 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

20 authors at 4 institutions in 3 countries.

Bin ZhouDepartment of Cardiology, Children’s Hospital Boston, Boston, Massachusetts, USA. zhoubin@sibs.ac.cn
Leah B Honor
Huamei He
Qing Ma
Jin-Hee Oh
Catherine Butterfield
Ruei-Zeng Lin
Juan M Melero-Martin
Elena Dolmatova
Heather S Duffy
Alexander von Gise
Pingzhu Zhou
Yong Wu Hu
Gang Wang
Bing Zhang
Lianchun Wang
Jennifer L Hall
Marsha A Moses
Francis X McGowan
William T Pu
Harvard University Press · USBoston Children's Hospital · USCatholic University of Korea · KRInstitute of Cardiology · PL

Funding

TUMOR DORMANCY INDUCED BY BLOCKED ANGIOGENESISP01CA045548 · NCI · CHILDREN'S HOSPITAL BOSTON · PI KLAGSBRUN, MICHAEL · 1987 to 2011
$22.6M
ZINC DEFICIENCY &PROTEIN EXPRESSION IN RAT OLFACTORY BULBSP41RR005351 · NCRR · UNIVERSITY OF GEORGIA (UGA) · PI VENOT, ANDRE · 1989 to 2011
$18.4M
Microenvironmental control of progenitors in organ dysfunction and repairU01HL100401 · NHLBI · UT SOUTHWESTERN MEDICAL CENTER · PI OLSON, ERIC N, SCHNEIDER, JAY W · 2009 to 2015
$8.3M
Epicardial progenitors in the developing and postnatal heartR01HL094683 · NHLBI · BOSTON CHILDREN'S HOSPITAL · PI PU, WILLIAM TSWENCHING · 2009 to 2016
$3.7M
Robo4 and heparan sulfate proteoglycan in angiogenesisR01HL093339 · NHLBI · UNIVERSITY OF SOUTH FLORIDA · PI WANG, LIANCHUN · 2009 to 2018
$3.4M
NCI NIH HHS P01 CA045548NCRR NIH HHS P41 RR005351NHLBI NIH HHS R01 HL093339NHLBI NIH HHS R01 HL094683NHLBI NIH HHS U01 HL100401
6 · The paper itself

Abstract

The epicardium makes essential cellular and paracrine contributions to the growth of the fetal myocardium and the formation of the coronary vasculature. However, whether the epicardium has similar roles postnatally in the normal and injured heart remains enigmatic. Here, we have investigated this question using genetic fate-mapping approaches in mice. In uninjured postnatal heart, epicardial cells were quiescent. Myocardial infarction increased epicardial cell proliferation and stimulated formation of epicardium-derived cells (EPDCs), which remained in a thickened layer on the surface of the heart. EPDCs did not adopt cardiomyocyte or coronary EC fates, but rather differentiated into mesenchymal cells expressing fibroblast and smooth muscle cell markers. In vitro and in vivo assays demonstrated that EPDCs secreted paracrine factors that strongly promoted angiogenesis. In a myocardial infarction model, EPDC-conditioned medium reduced infarct size and improved heart function. Our findings indicate that epicardium modulates the cardiac injury response by conditioning the subepicardial environment, potentially offering a new therapeutic strategy for cardiac protection.

Indexed as

AnimalsFibroblastsHeartHeart InjuriesHomeostasisIntercellular Signaling Peptides and ProteinsMiceModels, BiologicalModels, GeneticMyocardial InfarctionMyocardiumMyocytes, CardiacNeovascularization, PathologicPericardiumTreatment OutcomeIntercellular Signaling Peptides and Proteins

Identifiers

PMID21505261
PMCPMC3083761
OpenAlexW2132562087

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.