© 1999 by European Society of Cardiology
Copyright © 1999, European Society of Cardiology
Mechanisms of remodeling of gap junction distributions and the development of anatomic substrates of arrhythmias
aDepartment of Pathology, Washington University School of Medicine, Box 8118, 660 South Euclid Avenue, St. Louis, MO, 63110, USA
bDepartment of Surgery, Washington University School of Medicine, 660 South Euclid Avenue, St. Louis, MO, 63110, USA
cDepartment of Medicine, Washington University School of Medicine, 660 South Euclid Avenue, St. Louis, MO, 63110, USA
dCenter for Cardiovascular Research, Washington University School of Medicine, 660 South Euclid Avenue, St. Louis, MO, 63110, USA
saffitz@pathology.wustl.edu
* Corresponding author. Tel.: +1-314-362-7728; fax: +1-314-362-4096
Received 18 September 1998; accepted 10 December 1998
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1 Introduction |
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Alteration of structure (remodeling) is a fundamental response of the heart to injury or disease. It originates in changes in gene expression which, in turn, alter the types and amounts of regulatory and structural proteins in myocytes, the form and distribution of subcellular organelles (including the contractile apparatus and other specialized subcellular structures responsible for cardiac function), and changes in the structure of whole cells, the extracellular matrix and, ultimately, the tissue and whole organ. A change in cardiac structure inevitably leads to a change in cardiac function, but the complex relationships between altered structure and function are only beginning to be revealed. Although structural remodeling serves important adaptive purposes, maladaptive consequences of remodeling are likely to contribute to morbidity and mortality in patients with heart disease.
An important clinical setting in which altered structure begets altered function and in which responses to injury may serve adaptive purposes, but also
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2 Myocyte interconnections at gap junctions |
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3 Enhanced connexin expression and intercellular coupling as a component of the acute hypertrophic response |
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4 Redistribution of gap junctions in chronic heart disease |
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5 Alterations in connexin expression and distribution as a feature of myocytolysis |
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6 Connexin turnover and mechanisms of diminished coupling in chronic heart disease |
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7 Conclusions |
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