fig1

Figure 1. A scheme representing GSK-3β mediated cardiac senescence through inhibition of ULK-1 directed autophagy. Under basal conditions, phosphorylation of ULK1 at S913 by GSK-3β promotes autophagy. During aging, phosphorylation of GSK-3β at S9 prevents activation of ULK1, leading to inhibition of autophagy and stimulation of cardiac aging processes, including hypertrophy, fibrosis, apoptosis, and cardiac dysfunction.