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Here we established murine model of liver fibrosis and found that oroxylin A (40\u2009mg\/kg) could ameliorate angiogenesis in liver fibrosis may related to hypoxia inducible factor 1\u03b1 (HIF\u20101\u03b1). The underlying mechanism was further investigated by isolating and culturing murine primary LSECs. Hypoxia induced vascular endothelial growth factor A (VEGF\u2010A), angiopoietin 2 (Ang\u20102), and platelet endothelial cell adhesion molecule\u20101 (PECAM\u20101\/CD31) elevated in LSECs were reduced by oroxylin A or acriflavine (ACF, an HIF\u20101\u03b1 inhibitor), indicating HIF\u20101\u03b1 involved the angiogenesis of LSECs. Additionally, interference with Yes\u2010associated protein (YAP) significant downregulated the protein expression of HIF\u20101\u03b1 and VEGF\u2010A, while YAP plasmid exhibited an opposite effect. We next found that oroxylin A inhibited hypoxia\u2010induced nuclear translocation of YAP, which may influence the accumulation of HIF\u20101\u03b1 and subsequently decrease transcription of downstream target gene including VEGF\u2010A and Ang\u20102, thereby exerting an anti\u2010angiogenic activity.<\/jats:p><\/jats:sec>","DOI":"10.1002\/jcb.26388","type":"journal-article","created":{"date-parts":[[2017,8,31]],"date-time":"2017-08-31T08:12:23Z","timestamp":1504167143000},"page":"2258-2268","source":"Crossref","is-referenced-by-count":57,"title":["Oroxylin A prevents angiogenesis of LSECs in liver fibrosis via inhibition of YAP\/HIF\u20101\u03b1 signaling"],"prefix":"10.1002","volume":"119","author":[{"given":"Chenxi","family":"Zhang","sequence":"first","affiliation":[{"name":"Department of Pharmacology School of Pharmacy Nanjing University of Chinese Medicine Nanjing Jiangsu China"},{"name":"Jiangsu Key Laboratory for Pharmacology and Safety Evaluation of Chinese Materia Medica 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