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(Circulation Research. 2007;101:230.)
© 2007 American Heart Association, Inc.

Editorials

Periostin

More Than Just an Adhesion Molecule

Thomas K. Borg, Roger Markwald

From the Department of Cell and Developmental Biology and Anatomy (T.K.B.), University of South Carolina, Columbia; and the Department of Cell Biology and Anatomy (R.M.), Medical University of South Carolina, Charleston.

Correspondence to Thomas K. Borg, Department of Cell and Developmental Biology and Anatomy, University of South Carolina, Columbia 29208. E-mail Borg@med.sc.edu

See related article, pages 313–321

Key Words: heart • extracellular matrix • periostin

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

The form and function of the heart is determined by the dynamic interaction of both intra and extracellular signals. During normal growth of the neonatal heart myocytes undergo hypertrophy in response to variety of signals including changes in blood pressure^1–3. The number of fibroblasts also increase and the collagenous connective tissue is formed.^4,7,8 The coordination of these postnatal signals and cell interactions result in a heart that is adapted to adult function. However, in response to a changing environment, eg, hypertrophy, infarction, or failure, the normal coordination of between these signals becomes disrupted and leads to detrimental cardiac remodeling. Understanding the sources of these signals and their relationship to the myocyte and nonmyocyte populations of the ventricular wall would seemingly be an important key to understanding and regulating the adaptive processes that lead to altered cardiac function and potentially catastrophic failure.

It is well documented that the adaptive processes of cardiac remodeling are linked to dynamic myocyte-fibroblast interactions or cross-talk, including the expression of cytokines, ECM, as well as mechanical and electrical signals.^9,10 Whereas the myocyte population remains relatively stable, the fibroblasts, as in neonatal life, appear to change dramatically during hypertrophy and injury.¹¹ Of the various aspects of myocardial remodeling that have been explored in infarction, hypertrophy or congestive failure, most have centered on the changes in the extracellular compartment milieu, principally analyzing the changes in the amount of collagen and fibrosis. Correlative investigations have described the increases and alterations in the amount of collagen with changes in . . . [Full Text of this Article]

Related Article:

Genetic Manipulation of Periostin Expression Reveals a Role in Cardiac Hypertrophy and Ventricular Remodeling

Toru Oka, Jian Xu, Robert A. Kaiser, Jaime Melendez, Michael Hambleton, Michelle A. Sargent, Angela Lorts, Eric W. Brunskill, Gerald W. Dorn, II, Simon J. Conway, Bruce J. Aronow, Jeffrey Robbins, and Jeffery D. Molkentin
Circ. Res. 2007 101: 313-321. [Abstract] [Full Text] [PDF]

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