Research Perspective Volume 2, Issue 9 pp 627—631

Cellular senescence controls fibrosis in wound healing


Figure 2. A mechanistic model for CCN1-induced senescence. The binding of CCN1 to its receptors in fibro-blasts, integrin α6β1and HSPGs, activates RAC1 and the RAC1-dependent NADPH oxidase 1 to generate a robust and sustained accumulation of ROS. This leads to a DNA damage response and activation of p53, as well as the ROS-dependent hyperactivation of ERK and p38 MAPK, leading to p16INK4a induction [22]. Both p53 and p16INK4a act upon pRb to induce senescence.