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(Circulation Research. 2000;87:961.)
© 2000 American Heart Association, Inc.

Editorial

Whither Complexity in Myocardial Development?

Margaret L. Kirby

From the Institute of Molecular Medicine and Genetics, Medical College of Georgia, Augusta, Ga.

Correspondence to Margaret L. Kirby, PhD, Institute of Molecular Medicine and Genetics, Medical College of Georgia, Augusta, GA 30912-2640. E-mail mkirby@mail.mcg.edu

Key Words: myocardium • development • gene expression • domains

	Introduction

 
For anyone who has ever been on the sidelines during a discussion of congenital heart defects or had a few minutes to browse through Bharati and Lev’s 2-volume tome on heart malformations,¹ the complexity of cardiovascular development that underlies this pathology is painfully obvious. Our understanding of heart development in particular has lagged behind that of other more tidily developing organs that have the leisure of putting themselves together before they have to do anything. Perhaps it is for these reasons that the molecular age has come to heart development a bit slower and more painstakingly than to other systems.

The initial foray into heart development at the molecular level came from cell biologists, who had developed sophisticated reagents to study skeletal muscle contractile proteins and looked to the myocardium as another striated muscle. Gonzalez-Sanchez and Bader² developed the first antibodies that detected differences in myosin heavy chains in the developing chick heart. One antibody, MF20, is now used as a pan-myocardial marker in chick, and another was the first to specifically recognize only atrial myosin heavy chains. The same group quickly identified another myosin heavy chain that characterized the embryonic conduction system.³ This confirmed conventional wisdom from morphologists, who saw 3 types of myocardia: atrial, ventricular, and conduction (Purkinje). It additionally showed that differential expression of contractile protein isoforms occurred relatively early in development, well before the morphologists could see any differences. The regions of differential expression seemed rather flexible at first and could be altered epigenetically by agents . . . [Full Text of this Article]

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