Cardiac muscle is one of the least regenerative tissues in the body. Because most of the adult cardiomyocytes have lost their ability to regenerate, heart disease damage to cardiomyocytes is often unrepairable. In the United States, heart disease is the leading cause of death. How to improve the ability of the heart to repair itself has always been a problem for scientists. Recently, researchers at Baylor College of Medicine and the Texas Heart Institute explored pathways related to cardiac cell function and found the cause of heart repair. The study, published in Nature, provides a new strategy for promoting heart cell renewal. Professor James Martin, a senior author of the study, said: "We explored why myocardium cannot regenerate. In this study, we focus on two pathways in cardiomyocytes or cardiac cells: Hippo pathways involved in blocking adult cardiomyocyte turnover. And the dystrophin glycoprotein complex (DGC) pathway, which is critical for the normal function of cardiomyocytes. We also studied mutations in the DGC component, as patients with these mutations develop muscular dystrophy." Previous studies have shown that components of the DGC pathway may interact with members of the Hippo pathway in some way. In this study, Martin and colleagues studied the consequences of this interaction in animal models. Researchers use genetic engineering to make mice lack the genes involved in one or both of these pathways, and then determine the ability of the heart to repair damage. These studies show for the first time that dystroglycan 1 (a component of the DGC pathway) binds directly to Yap, a component of the Hippo pathway, and this interaction inhibits cardiomyocyte proliferation.
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