PI3K/AKT/mTOR通路
医学
腹主动脉瘤
血管紧张素II
自噬
蛋白激酶B
主动脉瘤
腹主动脉
血管平滑肌
主动脉
内科学
病理
信号转导
动脉瘤
细胞生物学
外科
生物
细胞凋亡
受体
生物化学
平滑肌
作者
Xianfeng Gu,Qi Li,Tianwei Qian,Qi Hu,Jianfeng Gu,Wei Ding,Ming Li,Ming Wang,Liu Huan,Kaixiang Tao
标识
DOI:10.1177/17085381231192688
摘要
Abdominal aortic aneurysm (AAA) is a potentially fatal vascular disorder with a high mortality rate. It was previously reported that fibroblast growth factor 21 (FGF21) was highly expressed in AAA patients. Nonetheless, its underlying mechanism in AAA progression is unclarified.Angiotensin II (Ang-II) was used to induce AAA in human aortic vascular smooth muscle cells (HASMCs) and mouse models. Western blotting and RT-qPCR were utilized for measuring protein and RNA levels. Immunofluorescence staining was utilized for detecting LC3B expression in HASMCs. Elastica van Gieson staining was conducted for histological analysis of the abdominal aortas of mice.FGF21 displayed a high level in Ang-II-stimulated HASMCs and AAA mice. FGF21 depletion ameliorated abdominal aorta dilation and Ang-II-triggered pathological changes in mice. FGF21 silencing hindered autophagy and PI3K/AKT/mTOR pathway.FGF21 contributes to AAA progression by enhancing autophagy and activating PI3K/AKT/mTOR pathway.
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