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J. Cardiovasc. Dev. Dis. 2014, 1(1), 98-110; doi:10.3390/jcdd1010098

Wnt/β-Catenin Signaling during Cardiac Development and Repair

Cardiovascular Research Center, Massachusetts General Hospital, Charles River Plaza, CPZN 3200, 185 Cambridge Street, Boston, MA 02114, USA
Harvard Medical School, 250 Longwood Avenue, Boston, MA 02115, USA
Department of Cardiology, University Medical Center Utrecht, Heidelberglaan 100, 3584 CX, Utrecht, The Netherlands
Harvard Stem Cell Institute, 1350 Massachusetts Avenue, Cambridge, MA 02138, USA
Authors to whom correspondence should be addressed.
Received: 21 February 2014 / Revised: 28 April 2014 / Accepted: 30 April 2014 / Published: 21 May 2014
View Full-Text   |   Download PDF [553 KB, 22 May 2014; original version 21 May 2014]   |  


Active Wnt/β-catenin signaling is essential for proper cardiac specification, progenitor expansion and myocardial growth. During development, the mass of the embryonic heart increases multiple times to achieve the dimensions of adult ventricular chambers. Cell division in the embryonic heart is fairly present, whereas cell turnover in the adult myocardium is extremely low. Understanding of embryonic cardiomyocyte cell-replication, therefore, could improve strategies for cardiac regenerative therapeutics. Here, we review which role Wnt signaling plays in cardiac development and highlight a selection of attempts that have been made to modulate Wnt signaling after cardiac ischemic injury to improve cardiac function and reduce infarct size.
Keywords: Wnt/β-catenin; heart; development; cardiomyocyte proliferation; regenerative medicine Wnt/β-catenin; heart; development; cardiomyocyte proliferation; regenerative medicine
This is an open access article distributed under the Creative Commons Attribution License (CC BY 3.0).

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MDPI and ACS Style

Buikema, J.W.; Zwetsloot, P.-P.M.; Doevendans, P.A.; Domian, I.J.; Sluijter, J.P.G. Wnt/β-Catenin Signaling during Cardiac Development and Repair. J. Cardiovasc. Dev. Dis. 2014, 1, 98-110.

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J. Cardiovasc. Dev. Dis. EISSN 2308-3425 Published by MDPI AG, Basel, Switzerland RSS E-Mail Table of Contents Alert
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