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Objective To explore the role and underlying mechanism of C1q/TNF-related protein 6 (CTRP6) in the development process of liver disease. Methods The histopathological examination and biochemical indexes of injured livers from wild-type (CTRP6+/+) and knockout (CTRP6-/-) mice induced by intragastric administration of CCl4 were analyzed. RT-qPCR was used to detect the expression of the fibrosis marker genes (Acta2, Col1al, Mmp2 and TGF-β) and cell proliferation marker genes (Cyclin D, Cyclin E and CDK6). Results Compared with CTRP6+/+ mice, the hepatocytes in CTRP6-/- mice showed mild necrosis, looseness and swelling. The high SOD activity and low MDA level were also observed in CTRP6-/- mice liver. Meanwhile, the expression of fibrosis and cell proliferation markers in CTRP6-/- mice were significantly lower than those in CTRP6+/+ mice. Conclusions CTRP6 gene is closely related to liver disease development, and the liver fibrosis progression induced by CCl4 is alleviated by its deletion. The mechanism may be explained as that CTRP6 knockout affects the proliferative capacity of hepatocytes.

This review mainly includes the following contents: 1) The multilevel of spatial topological structure of the fluid flow pathway is viewed from the transverse perspective (cross section), including perivascular space, basement membranes, tunica adventitia and perivascular connective tissue. And the diverse phenomenon of fluid flow at all levels of vascular structure is discussed; 2) The interstitial fluid flow in vascular trees throughout the whole body is viewed from the longitudinal perspective;3) The similarities and differences between domestic and foreign research results are compared;4) The potential physiological function of the interstitial fluid flow along the circulatory system is prospected.