This Article Full Text Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Request Permissions Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Epstein, J. A. Articles by Parmacek, M. S. Search for Related Content PubMed PubMed Citation Articles by Epstein, J. A. Articles by Parmacek, M. S. Related Collections Other myocardial biology Congestive Animal models of human disease Cardiac development

(Circulation. 2005;112:592-597.)
© 2005 American Heart Association, Inc.

Basic Science for Clinicians

Recent Advances in Cardiac Development With Therapeutic Implications for Adult Cardiovascular Disease

Jonathan A. Epstein, MD; Michael S. Parmacek, MD

From the Molecular Cardiology Research Center, Penn Cardiovascular Institute, University of Pennsylvania Health System, Philadelphia.

Correspondence to Jonathan A. Epstein, 954 BRB II, 421 Curie Blvd, Philadelphia, PA 19104. E-mail epsteinj@mail.med.upenn.edu

Key Words: heart defects, congenital • morphogenesis • myocytes • regeneration • stem cells

An extract of the first 250 words of the full text is provided, because this article has no abstract.

	Introduction

 
Congenital heart disease (CHD) is the most common birth defect in humans, occurring as often as 1 in 125 live births.^1,2 Because prenatal diagnosis and both medical and surgical care of affected neonatal infants have improved dramatically in the past decades, the number of adult survivors of CHD is increasing. Thus, it has become increasingly important for all cardiologists to be familiar with the basic and clinical characteristics of CHD. At the same time, there has been an explosion in our understanding of the molecular and genetic programs regulating cardiovascular development (for reviews, see Olson,³ Srivastava and Olson,⁴ and Gruber and Epstein⁵). Genetic causes of specific forms of CHD are appearing in the literature with increasing frequency. Interestingly, mutations in genes that encode nuclear transcription factors account for many forms of CHD. Here, we review examples of transcription factor gene mutations that cause human disease, and we address the potential utility of applying developmental insights to the study of adult cardiac regenerative therapy and to the development of novel treatment strategies for adult heart disease.

CHD most commonly arises from structural defects caused by errors in the morphogenetic programs regulating heart and outflow tract development. Less commonly, functional defects of cardiac muscle account for congenital cardiac disease such as occur in muscular dystrophies or storage diseases. These disorders are not discussed further here but have been reviewed by Cox and Kunkel,⁶ Emery,⁷ and Lapidos et al.⁸ Distinct and diverse structural abnormalities of the heart and cardiac outflow tract have . . . [Full Text of this Article]

This article has been cited by other articles:

				J. Cai, F.-F. Yi, L. Yang, D.-F. Shen, Q. Yang, A. Li, A. K. Ghosh, Z.-Y. Bian, L. Yan, Q.-Z. Tang, et al. Targeted Expression of Receptor-Associated Late Transducer Inhibits Maladaptive Hypertrophy via Blocking Epidermal Growth Factor Receptor Signaling Hypertension, March 1, 2009; 53(3): 539 - 548. [Abstract] [Full Text] [PDF]

				H.-L. Li, Z.-G. She, T.-B. Li, A.-B. Wang, Q. Yang, Y.-S. Wei, Y.-G. Wang, and D.-P. Liu Overexpression of Myofibrillogenesis Regulator-1 Aggravates Cardiac Hypertrophy Induced by Angiotensin II in Mice Hypertension, June 1, 2007; 49(6): 1399 - 1408. [Abstract] [Full Text] [PDF]

				K. E. Yutzey and J. Robbins Principles of Genetic Murine Models for Cardiac Disease Circulation, February 13, 2007; 115(6): 792 - 799. [Abstract] [Full Text] [PDF]