Reducing Cardiac Fibrosis: Na/K-ATPase Signaling Complex as a Novel Target

Cardiac fibrosis is a significant health issue and a common pathological process in cardiac disease that eventually leads to heart failure. Both experimental and clinical data have shown that formation of fibrotic scar tissue increases cardiac stiffness, whereas regression of fibrosis improves cardiac function. Several categories of drugs have been developed to treat cardiac fibrosis and cardiac failure in clinics. However, there remains a major gap in elucidating the mechanisms of cardiac fibrosis and its association with heart failure, which is still the leading cause of deaths in the United States. 

Therefore, the discovery of novel molecular targets is essential for improving patient outcomes. The Na/K-ATPase is an important transmembrane protein and is critical for maintaining ion homeostasis across the cell membrane. In the past 20 years, studies have revealed that the Na/K-ATPase can also complex with neighboring proteins and function as a signaling transducer that regulates a variety of signaling events such as the activation of Src kinase and NF?B, and the generation of reactive oxygen species