原癌基因酪氨酸蛋白激酶Src
炎症
磷酸化
内皮
达沙替尼
基因敲除
内皮功能障碍
酪氨酸激酶
细胞生物学
癌症研究
生物
免疫学
信号转导
内分泌学
细胞凋亡
生物化学
作者
Hanyi Ding,Minchun Jiang,Andrew M. Chan,Yin Xia,Ronald C.W.,Xiaoqiang Yao,Li Wang,Yü Huang
摘要
BACKGROUND AND PURPOSE: Previous studies have shown that Src can regulate inflammation and tumour progression. However, the mechanisms by which Src regulates the inflammatory response of vascular endothelium and atherogenesis are currently poorly understood. This study aimed to investigate the role of Src in endothelial inflammation and atherogenesis, as well as the underlying mechanisms. EXPERIMENTAL APPROACH: ; Cdh5-cre mice. Atherosclerosis was induced by partial ligation of the carotid artery. KEY RESULTS: mice induced by partial carotid artery ligation. Additionally, plaque formation was decreased in the ligated left carotid artery of mice with endothelial-specific Src knockdown. CONCLUSION AND IMPLICATIONS: Disturbed flow promotes endothelial inflammation and atherogenesis through the Piezo1-Src-Stat3 pathway. Therefore, inhibiting Src in endothelial cells could be a promising therapeutic strategy to treat atherogenesis. LINKED ARTICLES: This article is part of a themed issue Drugs and Drug Targets in Metabolic and Chronic Inflammatory Diseases. To view the other articles in this section visit http://onlinelibrary.wiley.com/doi/10.1111/bph.v182.20/issuetoc.
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