Fig. 16

The schematic diagram of MSCs against TGF-β1 induced fibrosis in HK-2 cells. On the one hand, MSCs maybe secrete any unknown cytokines which enter the cytoplasm through receptors, somehow bind to galectin-3, and inhibit phosphorylation of Akt (Ser473) and GSK3β (Ser9), next inhibiting downstream key EMT-inducing transcription factors, Snail. On the other hand, MSCs probably balance the ratio of TIMP1/MMP9 which regulates ECM generation and degradation. Ultimately, MSCs alleviate TGF-β1-inducing fibrosis in HK-2 cells. Further research is needed to explore which concrete cytokine secreted by MSCs interacts with galectin-3 and how to regulate the balance of TIMP1/MMP9