Tokyo Tech News
Published: May 31, 2009
Acute myocardial infarction is a frequent cause of chronic heart failure and is especially common in the industrialized nations. About 1.5 million individuals in the United States suffer acute myocardial infarction annually. We have found that the molecule periostin performs an essential function in repairing disrupted heart tissue after infarction.
The recruitment of fibroblastic cells to the infarct is essential to the cardiac healing process. Researchers have associated stiffness of the extracellular matrix in the infarcted myocardium with cardiac healing, but the molecular mechanism of cardiac healing remains unclear.
Periostin, we have shown, acts to recruit the cells that repair the defective cardiac muscle. We developed periostin-null mice and verified that the cardiac healing after acute myocardial infarction was conspicuously slower in those mice than in otherwise normal mice. Those and related findings that we have reported highlight the importance of activating periostin to promote cardiac healing after acute myocardial infarction.
M. Shimazaki, K. Nakamura, I. Kii, T. Kashima, N. Amizuka, M. Li, M. Saito, K. Fukuda, T. Nishiyama, S. Kitajima, Y. Saga, M. Fukayama, M. Sata, and A. Kudo
Journal of Experimental Medicine 205, pp. 295–303 (2008).
Department of Biological Information
This illustration depicts the periostin-induced migration of fibroblasts (white) to the border of an infarction, where they produce collagen fibers. The illustration is by Tokyo artist Kazue Murata (email@example.com).
Graduate School of Bioscience and Biotechnology Biological Information