Fig. 7
Schematic diagram illustrating the mechanisms underlying the effect of AMPKα1-mediated glycolysis on endothelial proliferation. Disturbed flow in atheroprone regions of blood vessels stimulates increased expression and activity of PRKAA1/AMPKα1 in ECs. Enhanced PRKAA1/AMPKα1 signaling promotes increased expression of HIF1A that, in turn, drives transcription of the glycolytic enzymes and consequently increased EC glycolysis. PRKAA1/AMPKα1-mediated glycolysis is vital to support increased proliferation of ECs and thus helps to preserve EC barrier integrity in vulnerable atheroprone regions and to protect from the infiltration of lipids and leukocytes into the vessel wall and the subsequent development and progression of atherosclerosis. The above protective mechanisms are compromised when the AMPKα1 pathway is blocked
