Engelhardt Stefan
Rudolf Virchow Center, DFG Research Center for Experimental Biomedicine, University of Würzburg, Würzburg, Germany.
J Clin Invest. 2007 Sep;117(9):2396-8. doi: 10.1172/JCI33135.
Acute stimulation of cardiac beta1-adrenergic receptors (beta1ARs) by norepinephrine represents the strongest endogenous mechanism for increasing cardiac function, but long-term stimulation induces cardiomyocyte apoptosis and contributes to cardiac disease. These effects have been attributed to coupling of the beta1AR to the stimulatory G protein (Gs) and classical cAMP-mediated signaling. In this issue of the JCI, Noma and colleagues report that cardiomyocyte beta1ARs may in addition deliver an antiapoptotic signal through transactivation of EGFRs (see the related article beginning on page 2445). Their findings provide a perspective for a novel class of receptor ligands that may direct beta1AR signaling toward alternative signaling pathways.
去甲肾上腺素对心脏β1 - 肾上腺素能受体（β1ARs）的急性刺激是增强心脏功能最强的内源性机制，但长期刺激会诱导心肌细胞凋亡并导致心脏疾病。这些效应归因于β1AR与刺激性G蛋白（Gs）的偶联以及经典的cAMP介导的信号传导。在本期《临床研究杂志》中，野间及其同事报告称，心肌细胞β1ARs可能还会通过表皮生长因子受体（EGFRs）的反式激活传递抗凋亡信号（见第2445页开始的相关文章）。他们的发现为一类新型受体配体提供了一个视角，这类配体可能将β1AR信号导向其他信号通路。
