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In mice with liver fibrosis produced by carbon tetrachloride (CCl<jats:sub>4<\/jats:sub>), the effects of olmesartan on intrahepatic angiogenesis and sinusoidal remodeling will be evaluated. <jats:italic>Methods<\/jats:italic>. By injecting CCl<jats:sub>4<\/jats:sub> into the peritoneal cavity, we established a mouse model of liver fibrosis. Using Sirius red and Masson trichrome staining, the extent of liver fibrosis in the animals was determined. Using immunohistochemical labeling and western blotting, the level of <jats:italic>\u03b1<\/jats:italic>\u2010smooth muscle actin (<jats:italic>\u03b1<\/jats:italic>\u2010SMA) expression, a characteristic of hepatic stellate cell activation, was assessed. Electron microscopy was used to determine the effect of olmesartan on hepatic sinusoidal capillarization, and immunohistochemical labeling was used to determine the expression levels of endothelial and basement membrane proteins in mouse liver tissues. Platelet\u2010derived growth factor (PDGF), IL\u201010, vascular endothelial growth factor (VEGF), and angiotensin II levels in mouse serum were measured by Luminex multifactor analysis and ELISA. Olmesartan\u2019s effect on the angiotensin II type 1 receptor (AT1R) and the VEGF receptor (VEGFR) was evaluated using western blotting. <jats:italic>Results<\/jats:italic>. Olmesartan reduced CCl<jats:sub>4<\/jats:sub>\u2010induced inflammatory cell infiltration and collagen deposition to alleviate liver fibrosis. <jats:italic>\u03b1<\/jats:italic>\u2010SMA expression was decreased, and HSC activation was inhibited in mouse liver tissues by olmesartan treatment. In addition, hepatic sinusoidal capillarization was improved under the action of olmesartan. The expression of collagen IV, fibronectin, CD31, and von Willebrand factor (VWF) in the olmesartan group was also markedly downregulated. In fibrotic mice, olmesartan medication decreased the levels of PDGF, VEGF, and angiotensin II, but it increased the level of IL\u201010. Moreover, olmesartan reduced the expression of VEGFR\u20101, VEGFR\u20102, and AT1R relative to CCl<jats:sub>4<\/jats:sub>\u2010induced liver fibrosis. <jats:italic>Conclusions<\/jats:italic>. In mice with CCl<jats:sub>4<\/jats:sub>\u2010induced fibrosis, olmesartan lowers angiogenesis and improves hepatic sinusoidal remodeling, according to our findings. By acting on the angiotensin II\u2010AT1R\u2010VEGF axis, this is achieved.<\/jats:p>","DOI":"10.1155\/2022\/4710993","type":"journal-article","created":{"date-parts":[[2022,8,26]],"date-time":"2022-08-26T22:05:09Z","timestamp":1661551509000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":5,"title":["Olmesartan Improves Hepatic Sinusoidal Remodeling in Mice with Carbon Tetrachloride\u2010Induced Liver 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