医学
自噬
下调和上调
安普克
PI3K/AKT/mTOR通路
心肌梗塞
癌症研究
小RNA
内科学
ULK1
血管平滑肌
冠状动脉
心脏病学
细胞凋亡
信号转导
激酶
细胞生物学
平滑肌
蛋白激酶A
动脉
生物
生物化学
基因
作者
Mei-Ying Xie,Yu-Tao Deng,Yuejun Huang,Lianjie Hou
标识
DOI:10.1016/j.ijcard.2022.08.004
摘要
Zhang et al. [1] reported that miR-145-5p is downregulated in blood and arteries specimens of patients with coronary stenosis. CaMKIIδ is promoted by the downregulation of miR-145-5p and then activating autophagy in human aortic vascular smooth muscle cells through the AMPK/mTOR/ULK1 signal pathway to regulate atherosclerosis progress. This finding may recognize a novel target of miR-145-5p in clinical therapy of atherosclerosis, whereas the mechanisms of miR-145-5p lowly expression in myocardial infarction need further exploration.
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