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The sympathetic nervous system promotes hepatic lymphangiogenesis, which is protective against liver fibrosis.

The liver is the largest lymph-producing organ. In cirrhotic patients, lymph production significantly increases concomitant with lymphangiogenesis. The aim of this study was to determine the mechanism of lymphangiogenesis in liver and its implication in liver fibrosis. Liver biopsies from portal hypertensive patients with portal-sinusoidal vascular disease(PSVD)(n=22) and liver cirrhosis(n=5) were evaluated for hepatic lymphatic vessels(LVs) comparing with controls(n=9, n=6, respectively). For mechanistic studies, rats with partial portal vein ligation(PPVL) and bile duct ligation(BDL) were used. Celiac ganglionectomy(CG) and 6-hydroxydopamine(6-OHDA) were used for sympathetic denervation. Finally, a gene profile dataset(GSE77627) including 14 histologically normal, 18 idiopathic non-cirrhotic portal hypertension(NCPH) and 22 cirrhotic patients was analyzed. Lymphangiogenesis was significantly increased in livers from PSVD patients, cirrhotic patients as well as PPVL and BDL rats. Importantly, Schwann cells of sympathetic nerves highly expressed VEGF-C in PPVL rats and promote lymphangiogenesis in vitro. VEGF-C neutralizing antibody or sympathetic denervation significantly decreased lymphangiogenesis in livers of PPVL and BDL rats, which resulted in progression of liver fibrosis. Liver specimens from cirrhotic patients showed a positive correlation between sympathetic nerve/Schwann cell positive areas and LV numbers, which was supported by gene set analysis from NCPH and cirrhotic patients. Sympathetic nerves promote hepatic lymphangiogenesis in non-cirrhotic and cirrhotic livers. Increased hepatic lymphangiogenesis can be protective against liver fibrosis.

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