AT1R expression increases with the degree of liver fibrosis, suggesting a role for angiotensin II in its development.
Should not change fibrosis management; hypothesis-generating for RAS inhibition in hepatic disease.
OBJECTIVE: To detect the expression of angiotensin II type 1 receptor (AT1R) in the different stages of human liver fibrosis. METHODS: The morphology and ultrastructure of hepatic stellate cells (HSC) in hepatic sinusoids were studied by transmission electron microscopy, collagen I (col I) was tested by immunohistochemical method, an indirect immunofluorescence labeling method was used to detect AT1R, and semiquantitative RT-PCR was used to detect AT1R mRNA. RESULTS: Positive expression of AT1R was mainly distributed in the periphery of hepatic lobules and in the cytoplasm of HSC in the sinusoids. In normal liver tissue from 12 cases, positive expression of AT1R was seen in 8, whereas in 18 fibrotic livers, all showed positive expression. Cells that positively expressed AT1R were significantly more abundant in the fibrotic liver group than in the normal liver group (P < 0.001), and were significantly increased with an increase in the collagenous surface area. The relative expression level of AT1R mRNA in the fibrotic liver group was also higher than in the normal liver group (P < 0.01). CONCLUSIONS: The expressions of both AT1R and AT1R mRNA increased significantly with the degree of liver fibrosis, so angiotensin II and its receptor are probably important in the development of liver fibrosis.
No takes yet. Share an insight, caveat, or question.
Wang et al. (2004) studied this question.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: