Differences between physiological and pathological cardiac hypertrophy offer new strategies for treating heart failure

无论是运动员还是心脏病患者和心力衰竭患者，心脏都会变大。在第一种情况下，大的（肥大的）心脏具有正常或甚至增加的泵送能力（功能），而在患有心脏病的患者中，功能被抑制并且心脏可能衰竭。我的研究是为了找出这两种情况的区别，以及是什么机制导致一个大心脏泵得很好，另一个大心脏泵得很差。具体来说，我的项目希望确定造成差异的基因和蛋白质。我已经发现了一个这样的基因，我现在计划通过在患有心力衰竭的动物（转基因小鼠）中过表达来操纵这个基因。我预测该基因的过度表达将改善心力衰竭模型的心脏功能。如果这一假设是正确的，那么激活运动员心脏中被激活的基因可能是改善心力衰竭患者心脏功能、生活质量和寿命的潜在工具。

The heart becomes large both in athletes as well as in patients with heart disease and failure. In the first instance, the large (hypertrophied) heart has normal or even increased pumping ability (function) whereas in the patient with heart disease the function is depressed and the heart may fail. My studies are directed towards finding out what is the difference in these 2 situations and what mechanisms are responsible for making one big heart pump well and the other big heart pump poorly. Specifically my project hopes to identify the genes and proteins responsible for the differences. I have already identified one such gene and I now plan to manipulate this gene by overexpressing it in animals (transgenic mice) with heart failure. I predict that overexpression of this gene will improve heart function in models of heart failure. If the hypothesis is correct, activating genes that are activated in the athlete's heart maybe a potential tool for improving heart function, quality of life and life span in patients with heart failure.