Fig 2: Schematic diagram illustrating the mechanisms underlying the effect of AMPKa1-mediated glycolysis on endothelial proliferation. Disturbed flow in atheroprone regions of blood vessels stimulates increased expression and activity of PRKAA1/AMPKa1 in ECs. Enhanced PRKAA1/AMPKa1 signaling promotes increased expression of HIF1A that, in turn, drives transcription of the glycolytic enzymes and consequently increased EC glycolysis. PRKAA1/AMPKa1-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 AMPKa1 pathway is blocked

Fig 3: Kaplan-Meier survival curves of disease-free survival. (A and B) Survival analysis based on (A) AMPK and (B) TET2 expression levels. AMPK, AMP-activated protein kinase; TET2, ten-eleven translocation 2.

Fig 4: Kaplan-Meier survival curves of overall survival. (A and B) Survival analysis based on (A) AMPK and (B) TET2 expression levels. AMPK, AMP-activated protein kinase; TET2, ten-eleven translocation 2.

Fig 5: Immunohistochemical staining of the expression levels of AMPK and TET2 in CRC specimens. (A-D) AMPK and (F-H) TET2 proteins were mainly detected in the cytoplasm and membrane of CRC cells. Representative staining patterns of CRC with (A and E) negative, (B and F) weak, (C and G) moderate and (D and H) strong staining intensity. Magnification, ×200. CRC, colorectal cancer; AMPK, AMP-activated protein kinase; TET2, ten-eleven translocation 2.