Fig. 7.

Working model of ADSC-derived exosomes in liver fibrosis. When DEN/CCl₄-induced liver fibrosis occurred, HSCs cells were activated and highly proliferated, and then, ECM deposition was facilitated. Moreover, glutamine synthetase-positive subset cells of perivenous hepatocytes were dysregulated, which are manifested as two key enzymes for glutamine production OAT and Glul down-regulated, leading to ammonia metabolic homeostasis in liver broken and accelerating hepatic dysfunctions in liver fibrosis. However, our study demonstrated that ADSC-EXO treatment could suppress HSCs activation and weak its proliferation ability, then accompanying with ECM deposition remission. Importantly, ADSC-EXO treatment could restore ammonia metabolic homeostasis by up-regulating OAT and Glul of perivenous hepatocytes. Overall, ADSC-EXO led to hepatic functions recovery in hepatic fibrosis disease