The Role of the Epicardium During Heart Development and Repair.


Journal

Circulation research
ISSN: 1524-4571
Titre abrégé: Circ Res
Pays: United States
ID NLM: 0047103

Informations de publication

Date de publication:
31 01 2020
Historique:
entrez: 31 1 2020
pubmed: 31 1 2020
medline: 25 7 2020
Statut: ppublish

Résumé

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.

Identifiants

pubmed: 31999538
doi: 10.1161/CIRCRESAHA.119.315857
pmc: PMC7000171
mid: NIHMS1549192
doi:

Types de publication

Journal Article Research Support, N.I.H., Extramural Research Support, Non-U.S. Gov't Review

Langues

eng

Sous-ensembles de citation

IM

Pagination

377-394

Subventions

Organisme : NHLBI NIH HHS
ID : R01 HL136179
Pays : United States
Organisme : NCATS NIH HHS
ID : UL1 TR002001
Pays : United States
Organisme : NHLBI NIH HHS
ID : T32 HL007572
Pays : United States
Organisme : NHLBI NIH HHS
ID : R01 HL133761
Pays : United States
Organisme : NIGMS NIH HHS
ID : T32 GM068411
Pays : United States
Organisme : NHLBI NIH HHS
ID : R01 HL144867
Pays : United States
Organisme : NHLBI NIH HHS
ID : R01 HL120919
Pays : United States
Organisme : NHLBI NIH HHS
ID : F32 HL134206
Pays : United States
Organisme : NHLBI NIH HHS
ID : T32 HL066988
Pays : United States
Organisme : Howard Hughes Medical Institute
Pays : United States

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Auteurs

Pearl Quijada (P)

From the Aab Cardiovascular Research Institute (P.Q., E.M.S.), University of Rochester, School of Medicine and Dentistry, Rochester, NY.
Department of Medicine (P.Q., E.M.S.), University of Rochester, School of Medicine and Dentistry, Rochester, NY.

Michael A Trembley (MA)

Department of Cardiology, Boston Children's Hospital, MA (M.A.T.).

Eric M Small (EM)

From the Aab Cardiovascular Research Institute (P.Q., E.M.S.), University of Rochester, School of Medicine and Dentistry, Rochester, NY.
Department of Medicine (P.Q., E.M.S.), University of Rochester, School of Medicine and Dentistry, Rochester, NY.

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