基因敲除
急性肾损伤
下调和上调
小RNA
长非编码RNA
细胞凋亡
癌症研究
缺血性损伤
医学
肾
缺血
细胞生物学
生物
基因
内科学
生物化学
作者
Jing Liu,Xiaozhou Li,Jurong Yang,Dongshan Zhang
出处
期刊:Apoptosis
[Springer Nature]
日期:2022-05-26
卷期号:27 (7-8): 531-544
被引量:12
标识
DOI:10.1007/s10495-022-01730-3
摘要
Although previous studies have revealed that long noncoding RNAs (lncRNAs) regulate the progression of ischemic acute kidney injury (AKI), the exact role and mechanism of lncRNA ENSMUST_147219 in ischemic AKI are not clear. In the present study, lncRNA ENSMUST_147219 was induced by ischemic injury in vitro and in vivo. Functionally, lncRNA ENSMUST_147219 mediated apoptosis in mouse proximal tubule-derived cell line (BUMPT). Mechanistically, lncRNA ENSMUST_147219 sponged the microRNA (miR)-221-5p to upregulate the expression of interferon regulatory factor 6 (IRF6) to drive apoptosis. Finally, knockdown of lncRNA ENSMUST_147219 markedly attenuated the ischemic AKI by targeting the miR-221-5p/IRF6 axis. Collectively, our data demonstrated that lncRNA ENSMUST_147219 promoted the development of ischemic AKI by regulating the miR-221-5p/IRF6 pathway, which could be considered a new therapeutic target for ischemic AKI.
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