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(Circulation Research. 2002;91:556.)
© 2002 American Heart Association, Inc.

Editorials

JNK Bond Regulation

Why Do Mammalian Hearts Invest in Connexin43?

Ralph J. Barker, Robert G. Gourdie

From the Department of Cell Biology and Anatomy, Medical University of South Carolina, Charleston, SC.

Correspondence to Dr Robert G. Gourdie, Dept of Cell Biology and Anatomy, MUSC, 173 Ashley Ave, Suite 601, Charleston, SC 29425. E-mail gourdier@musc.edu

Key Words: human • gap junction • disease • c-Jun N-terminal kinase • transgenic

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

Large numbers of gap junctions interconnect working myocytes in the ventricle of adult humans.^1–5 Until recently, it was assumed that the reason for the abundance of these clusters of intercellular channels was straightforward. This phenomenon was thought to be principally a matter of ensuring that action potentials were conducted efficiently from myocyte to myocyte.^6–8 However, it has long been known that the mammalian heart is atypical with respect to that of other vertebrates in the high frequency and large size of gap junctions found between its constituent muscle cells.^1–5,9,10 In nonmammalian chordates ranging from the affixed sea-squirt¹⁰ to the nimble sparrow,⁹ spread of activation is expedited and maintained in the main pumping chamber of the heart with only a fraction of the channels that are apparently required in humans.

The molecular composition of gap junction channels in the adult mammalian ventricle is also a phylogenetic oddity. By far, the most abundantly expressed subunit protein of the numerous gap junctions found in this tissue is connexin43 (Cx43),^1–8,10,11 a member of the connexin family of proteins that is probably all but absent from the mature cardiac muscle of other species on the vertebrate family tree.¹⁰ Thus, of the many species and classes of animal within our phylum, we mammals seem literally to be out on a limb in terms of the characteristics of the electrotonic couplings linking our ventricular muscle cells.

In addition to being expressed at high levels in the mammalian ventricle, significant resources are allocated to regulation of the trafficking, . . . [Full Text of this Article]

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