Von Willebrand factor deficiency reduces liver fibrosis in mice

摘要: Liver diseases are associated with complex changes in the hemostatic system and elevated levels of platelet-adhesive protein Von Willebrand factor (VWF) reported patients acute chronic liver damage. Although VWF fibrosis general population, role injury has not been examined depth experimental settings. We tested hypothesis that deficiency inhibits fibrosis. Wild-type (WT) VWF-deficient mice were challenged carbon tetrachloride (CCl4) impact on was determined. did significantly affect CCl4-induced hepatocellular necrosis mice. Chronic CCl4 challenge, twice weekly for 6 weeks, increased hepatic stellate cell activation collagen deposition livers WT Interestingly, induction several profibrogenic genes attenuated Moreover, birefringent sirius red staining (indicating type I III collagens) immunofluorescence indicated a reduction CCl4-exposed compared to The results indicate attenuates without affecting necrosis. first demonstrate reduces progression fibrosis, suggesting mechanistic plasma cirrhosis.