doi: 10.1161/01.ATV.0000125707.94116.a4
© 2004 American Heart Association, Inc.
Editorials |
Role of Renin Angiotensin System in Angiogenesis: It Is Still Elusive
From the Department of Cardiovascular Medicine, Kyushu University Graduate School of Medical Sciences, Fukuoka, Japan.
Correspondence to Toshihiro Ichiki, Department of Cardiovascular Medicine, Kyushu University Graduate School of Medical Sciences, 3-1-1 Maidashi, Higashi-ku 812-8582 Fukuoka, Japan. E-mail ichiki@cardiol.med.kyushu-u.ac.jp
An extract of the first 250 words of the full text is provided, because this article has no abstract. |
Neovascularization is an integral component of the cardiac remodeling process after myocardial infarction. Numerous and dilated vessels appear in the border zone of infarcted and noninfarcted area after experimental myocardial infarction.1 As a result, coronary vasodilatory capacity resumes to the normal level after several weeks of infarction by an increase in blood flow in the proximal region of the infarcted myocardium. However, it is generally believed that neovascularization after myocardial infarction is limited and insufficient to preserve viable myocardium of the border zone area. A number of clinical and experimental trials of therapeutic angiogenesis, therefore, have been performed to improve cardiac function and survival after myocardial infarction. Several methods including administration of angiogenic growth factors and injection of naked DNA or virus vector that expresses angiogenic factors have been employed. Recent studies have shown that transplantation of bone marrow-derived angioblasts and mesenchymal stem cells are a promising source for tissue regeneration and repair, including neovascularization after myocardial infarction.2,3 Indeed these studies indicated that cardiac function was improved by administration of these progenitor cells, suggesting that neovascularization after myocardial inaction may be beneficial for the infarcted heart. In this issue of Arteriosclerosis, Thrombosis, and Vascular Biology, however, the findings of Toko et al4 challenge this view. Toko et al4 show that less neovascularization was induced in AT1a-deficient mice compared with wild type mice after myocardial infarction. It is generally accepted that blockade of the Angiotensin (Ang) II type 1 receptor (AT1) preserves cardiac function after myocardial infarction, and the authors
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