Proteomic analysis of the cardiac myocyte secretome reveals extracellular protective functions for the ER stress response.
Simultaneous Isolation and Culture of Atrial Myocytes, Ventricular Myocytes, and Non-Myocytes from an Adult Mouse Heart.
The ER Unfolded Protein Response Effector, ATF6, Reduces Cardiac Fibrosis and Decreases Activation of Cardiac Fibroblasts.
Pharmacologic ATF6 activation confers global protection in widespread disease models by reprograming cellular proteostasis.
ATF6 Decreases Myocardial Ischemia/Reperfusion Damage and Links ER Stress and Oxidative Stress Signaling Pathways in the Heart.