Send to

Choose Destination

The Role of the Epicardium in the Formation of the Cardiac Valves in the Mouse.


Etiology and Morphogenesis of Congenital Heart Disease: From Gene Function and Cellular Interaction to Morphology [Internet]. Tokyo: Springer; 2016. Chapter 20.
2016 Jun 25.

Author information

Department of Pediatric Cardiology, Tokyo Women's Medical University, Tokyo, Japan
Cardiovascular Developmental Biology Center, Medical University of South Carolina Clemson University, Charleston, South Carolina, USA
Department of Pediatrics (Cardiology), Vanderbilt University, Nashville, Tennessee, USA
Pediatrics, Pharmacology and Toxicology, and Bioengineering, University of Louisville, Louisville, Kentucky, USA
Gladstone Institute of Cardiovascular Disease, San Francisco, California, USA
Pediatrics, Division of Pediatric Cardiology, Keio University School of Medicine, Tokyo, Japan
Department of Regenerative Medicine and Cell Biology, Medical University of South Carolina, 173 Ashley Avenue, Room BSB-648B, 250508, Charleston, SC, 29425, USA
Department of Anatomy, Embryology and Physiology, Academic Medical Center, Heart Failure Research Center, Meibergdreef 15, Amsterdam, 1105AZ, The Netherlands


In recent years, insights into the role of the epicardium in cardiac development have significantly changed. An important contribution to this increasing knowledge comes from the availability of mouse models that facilitate the study of the fate of the epicardial cell lineage and that allow epicardial-specific manipulation of expression of genes involved in regulation of epicardial cell behavior. In this contribution we will discuss our growing understanding of the role of the epicardium and epicardially derived cells in the formation of the atrioventricular valve leaflets. We will illustrate how epicardially derived cells specifically contribute to the development of the leaflets that derive from the lateral atrioventricular cushions, and we will discuss the role of Bmp signaling, through the Bmp receptor BmpR1A/Alk3, in the regulation of the preferentially migration of EPDCs into the parietal AV valve leaflets.

Copyright 2016, The Author(s).

Support Center