Figure 2.

Effects of high glucose on fibroblast activity and fibrotic function of different organs. Several different mechanisms of diabetic fibrosis: 1) the activation of neurohumoral pathways, 2) induction and activation of growth factors such as TGF–β and platelet–derived growth factors, 3) stimulation of pro–inflammatory cytokines such as TNF–α and IL–1β. The main pathway that fibroblasts activate in response to high glucose involves ROS production, 4) high glucose can aggravate the damage of ROS to cells, promote cell senescence, and cause chronic inflammation and fibrosis. Ang II, angiotensin II, ROS, reactive oxygen species, PDGFs, platelet–derived growth factors, IL–β, interleukin–β, TNF–α, tumor necrosis factor α.