Takaaki Senbonmatsu, Sahoko Ichihara, Edward Price, F. Andrew Gaffney, Tadashi Inagami
J Clin Invest.
2000;
106(3):R25–R29
doi:10.1172/JCI10037
This article Copyright © 2000, The American Society for Clinical Investigation
Abstract
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T
he pathophysiological roles of the angiotensin II type 2 receptor (AT2) in cardiac hypertrophy remain unclear. By the targeted deletion of mouse AT2 we were able to prevent the left ventricular hypertrophy resulting from pressure overload, while cardiac contractile functions remained normal. This implies that AT2 is a mediator of cardiac hypertrophy in response to increased blood pressure. The effects of AT2 deletion were independent of activation of embryonic genes for cardiac hypertrophy. However, p70S6k, one of the key factors in cardiac hypertrophy, was markedly and specifically reduced in the ventricles of Agtr2–/Y mice. We propose that p70S6k plays a major role in AT2-mediated ventricular hypertrophy.This article may have been published online in advance of the print edition. The date of publication is available from the JCI website, http://www.jci.org. J. Clin. Invest. 105:R25–R29 (2000).
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