Fig. 2.

Effects of AngII on the TGF-β/SMAD signaling pathway, inflammation, OS and fibrosis pathway. Binding of ANGII to AT1R, irritate MAPK complex to activate SMAD complex to enter the nucleus and express fibrotic genes. NF-kB activated by AngII/AT1R interaction increase the expression of molecules related to inflammation. AngII up-regulates the expression of NOX that help to increase of OS. These pathological conditions are parallel with adhesion formation post-surgical pathogenesis. NF-kB, nuclear factor kappa B; TGF-β, transforming growth factor β; OS, oxidative stress; NOX, NADH oxidase; AngII/AT1R angiotensin II/angiotensin II type 1 receptor; ROS, reactive oxygen species.