UC San Diego

As the number one cause of death in the world, and the leading cause of death in the United States, heart disease claims more lives than all forms of cancer combined (Go et al., 2013). Though several therapies are available to

alleviate its symptoms and delay the progression of cardiac deterioration, there is currently no cure for heart failure. The discovery of new proteins and pathways, and understanding their mechanisms, create targets for potential therapeutic approaches.

Calcium and β-adrenergic receptor (β-AR) signaling are both important factors in cardiac function. Here, we examined CREB Regulated Transcriptional Co-activator 2 (CRTC2), a known converging point between β-adrenergic receptor and calcium in glucose metabolism. Little is known about the function of CRTC2 in cardiomyocytes. Upon comparison of survival and cardiac function of wildtype and transgenic nuclear targeted CRTC2 (ntCRTC2) mice in the setting of chronic heart failure (CHF), we provide evidence of trends favoring mice with upregulated ntCRTC2. Understanding of a β-AR and calcium point of convergence will enable development of de novo treatments that modulate both systems, both of which are fundamental to cardiac function.