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Page 4 of 6                                                       Lin et al. Hepatoma Res 2018;4:48  I  http://dx.doi.org/10.20517/2394-5079.2018.19


























                         Figure 1. Scatter plot demonstrating the slope of CHI3L1 concentration and fibrosis progression rate per year


                                   Water inlet
                                    (fibrosis
                                  progression)









                                  Water levels
                                 (fibrosis degree
                                   or stages)





                                                                             Water outlet
                                                                           (fibrosis regression)

                    Figure 2. A water tank model to describe the relationship between the progression or regression of liver fibrosis and CHI3L1


               CONCLUSION
               CHI3L1 is not only a staging marker for fibrosis in treatment naïve HBV- or HCV-infected patients and
               NAFLD patients. CHI3L1 is also predictive of progression or regression of fibrosis. These abilities are
               likely due to the fact that CHI3L1 is actively involved in the process of liver fibrosis. Johansen et al.  used
                                                                                                    [15]
               immunohistochemical analysis to demonstrate that CHI3L1 is expressed in areas with fibrosis, particularly
               leading edges/areas with active fibrogenesis. CHI3L1 staining was not observed in hepatocytes but was
               expressed in Kupffer cells  and potentially hepatic stellate cells (HSC) . He et al.  demonstrated that
                                      [6]
                                                                             [15]
                                                                                       [16]
               CHI3L1 binds to interleukin-13 receptor α2 (IL-13Rα2), activates MAPK (macrophage mitogen-activated
               protein kinase), protein kinase B/AKT, and Wnt/β-catenin signaling, and regulates TGF-β1 production via
               IL-13Rα2-dependent mechanisms. CHI3L1 also promotes HSC activation and proliferation .
                                                                                            [4]
               Here, we present a water tank model [Figure 2] to explain the relationship between the progression or
               regression of liver fibrosis and the concentration and increasing speed of CHI3L1. The inlet of water
               represents the parameters of CHI3L1, and the girth of the inlet pipe represents the absolute concentration of
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