Evidence map›Paper›PMID 31999538›Full record

ReviewCirculation research2020

The Role of the Epicardium During Heart Development and Repair.

Pearl Quijada, Michael A Trembley, Eric M Small

Open access · bronzeAbstract readReview
In one paragraph

Review in Circulation research, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 139 papers.

0numbers the graph read from it
0cells of the map it votes in
139citing papers in PubMed
9.6field-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

139 citing papers in PubMed, 194 citations in OpenAlex.

  1. Article
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  14. RNA-Binding Protein Trim71 Controls Epicardial Cell Migration.Journal of cardiovascular development and disease · 2026
    Article
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79 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

3 authors at 1 institution in 1 country.

Pearl QuijadaFrom the Aab Cardiovascular Research Institute (P.Q., E.M.S.), University of Rochester, School of Medicine and Dentistry, Rochester, NY.
Michael A TrembleyDepartment of Cardiology, Boston Children's Hospital, MA (M.A.T.).
Eric M SmallFrom the Aab Cardiovascular Research Institute (P.Q., E.M.S.), University of Rochester, School of Medicine and Dentistry, Rochester, NY.
University of Rochester · US

Funding

The University of Rochester's Clinical and Translational Science InstituteUL1TR002001 · NCATS · UNIVERSITY OF ROCHESTER · PI WILSON, KAREN M., ZAND, MARTIN S · 2016 to 2024
$34.6M
RESEARCH METHODS IN PEDIATRICS HEART DISEASET32HL007572 · NHLBI · CHILDREN'S HOSPITAL BOSTON · PI Sarah D DE FERRANTI, Jane W. Newburger · 1985 to 2026
$13.0M
MULTIDISCIPLINARY TRAINING IN PULMONARY RESEARCHT32HL066988 · NHLBI · UNIVERSITY OF ROCHESTER · PI GEORAS, STEVE N, O'REILLY, MICHAEL A · 2001 to 2021
$8.1M
Training in Cellular, Biochemical and Molecular SciencesT32GM068411 · NIGMS · UNIVERSITY OF ROCHESTER · PI MAQUAT, LYNNE E · 2005 to 2019
$3.9M
Role of PKP2 in epicardial structure and functionR01HL136179 · NHLBI · NEW YORK UNIVERSITY SCHOOL OF MEDICINE · PI DELMAR, MARIO, MORLEY, GREGORY E · 2017 to 2020
$3.1M
Dysregulation of common metabolic and transcriptional pathways in heart and lung fibrosisR01HL133761 · NHLBI · UNIVERSITY OF ROCHESTER · PI SMALL, ERIC M, WOELLER, COLLYNN FREMONT · 2016 to 2019
$2.1M
Regulation of epicardial cell differentiation during development and diseaseR01HL120919 · NHLBI · UNIVERSITY OF ROCHESTER · PI SMALL, ERIC M · 2014 to 2018
$1.9M
Coordination of inflammatory signaling and cardiac fibrosis by small proline rich proteinsR01HL144867 · NHLBI · UNIVERSITY OF ROCHESTER · PI SMALL, ERIC M · 2019 to 2022
$1.7M
Novel mechanisms of epicardium dependent cardiac repairF32HL134206 · NHLBI · UNIVERSITY OF ROCHESTER · PI QUIJADA, PEARL JENNINE · 2016 to 2018
$122k
Howard Hughes Medical InstituteNCATS NIH HHS UL1 TR002001NHLBI NIH HHS F32 HL134206NHLBI NIH HHS R01 HL120919NHLBI NIH HHS R01 HL133761NHLBI NIH HHS R01 HL136179NHLBI NIH HHS R01 HL144867NHLBI NIH HHS T32 HL007572NHLBI NIH HHS T32 HL066988NIGMS NIH HHS T32 GM068411
6 · The paper itself

Abstract

The heart is lined by a single layer of mesothelial cells called the epicardium that provides important cellular contributions for embryonic heart formation. The epicardium harbors a population of progenitor cells that undergo epithelial-to-mesenchymal transition displaying characteristic conversion of planar epithelial cells into multipolar and invasive mesenchymal cells before differentiating into nonmyocyte cardiac lineages, such as vascular smooth muscle cells, pericytes, and fibroblasts. The epicardium is also a source of paracrine cues that are essential for fetal cardiac growth, coronary vessel patterning, and regenerative heart repair. Although the epicardium becomes dormant after birth, cardiac injury reactivates developmental gene programs that stimulate epithelial-to-mesenchymal transition; however, it is not clear how the epicardium contributes to disease progression or repair in the adult. In this review, we will summarize the molecular mechanisms that control epicardium-derived progenitor cell migration, and the functional contributions of the epicardium to heart formation and cardiomyopathy. Future perspectives will be presented to highlight emerging therapeutic strategies aimed at harnessing the regenerative potential of the fetal epicardium for cardiac repair.

Indexed as

RegenerationAnimalsHeart DiseasesHumansMyocardiumParacrine CommunicationPericardiumfibrosisgrowth and developmentmyocardial ischemiaparacrine communicationregeneration

Identifiers

PMID31999538
PMCPMC7000171
OpenAlexW3003280117

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.