Dorn Gerald W, Force Thomas
Heart and Vascular Center, Medical Center, University of Cincinnati, Cincinnati, Ohio 45267-0542, USA.
J Clin Invest. 2005 Mar;115(3):527-37. doi: 10.1172/JCI24178.
In broad terms, there are 3 types of cardiac hypertrophy: normal growth, growth induced by physical conditioning (i.e., physiologic hypertrophy), and growth induced by pathologic stimuli. Recent evidence suggests that normal and exercise-induced cardiac growth are regulated in large part by the growth hormone/IGF axis via signaling through the PI3K/Akt pathway. In contrast, pathological or reactive cardiac growth is triggered by autocrine and paracrine neurohormonal factors released during biomechanical stress that signal through the Gq/phospholipase C pathway, leading to an increase in cytosolic calcium and activation of PKC. Here we review recent developments in the area of these cardiotrophic kinases, highlighting the utility of animal models that are helping to identify molecular targets in the human condition.
广义而言，有三种类型的心肌肥大：正常生长、由体育锻炼诱导的生长（即生理性肥大）以及由病理刺激诱导的生长。最近的证据表明，正常和运动诱导的心脏生长在很大程度上受生长激素/胰岛素样生长因子轴通过PI3K/Akt途径的信号传导调节。相比之下，病理性或反应性心脏生长是由生物力学应激期间释放的自分泌和旁分泌神经激素因子触发的，这些因子通过Gq/磷脂酶C途径发出信号，导致胞质钙增加和蛋白激酶C激活。在此，我们综述了这些心肌营养激酶领域的最新进展，强调了有助于确定人类疾病分子靶点的动物模型的实用性。
