Figure 7.

Schematic summary of the signalling pathway underlying the senescence of HAECs induced by downregulation of B‐myb. Knockdown of B‐myb by siB‐myb upregulates p22^phox, which can promote ROS production in primary cultured HAECs. Excessive ROS accumulation can activate p53/p21 pathway which is the major pathway of senescence, causing further cellular senescence. The upregulation of p53 and p21 can be blocked by ROS scavenger NAC or specific p53 inhibitor PFTα in B‐myb knockdown‐induced senescence. These findings suggest that activation of ROS/p53/p21 signalling pathway is involved in B‐myb knockdown‐induced senescence in HAECs