Periostin: more than just an adhesion molecule.

See related article, pages 313–321 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 pressure1–3. 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 …