医学
发病机制
下调和上调
自噬
小RNA
安普克
冠状动脉疾病
PI3K/AKT/mTOR通路
血管平滑肌
疾病
内科学
癌症研究
信号转导
平滑肌
细胞生物学
激酶
蛋白激酶A
基因
细胞凋亡
化学
生物
生物化学
作者
Gang Zhou,Hui Wu,Di Liu,Yunzhao Li,Zhao Dong
标识
DOI:10.1016/j.ijcard.2022.07.014
摘要
Recently, we have read with great interest the published paper by Zhang et al. [1], who found that the expression of miR-145-5p was downregulated in blood and artery specimens of patients with coronary stenosis. They further showed that downregulation of miR-145-5p could enhance CaMKIIδ expression in human aortic vascular smooth muscle cells and then activate autophagy through the AMPK/mTOR/ULK1 pathway to promote the formation of atherosclerosis. This result indicated that miR-145-5p played a critical role in the pathogenesis of atherosclerosis.
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