LncRNA TUG1 attenuates ischaemia-reperfusion-induced apoptosis of renal tubular epithelial cells by sponging miR-144-3p via targeting Nrf2.
LncRNA TUG1 attenuates ischaemia-reperfusion-induced apoptosis of renal tubular epithelial cells by sponging miR-144-3p via targeting Nrf2.
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LncRNA TUG1 通过靶向 Nrf2 海绵 miR-144-3p 减弱缺血再灌注诱导的肾小管上皮细胞凋亡
DOI:
10.1111/jcmm.16924
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发表时间:
2021-10
影响因子:
5.3
通讯作者:
Cheng F
中科院分区:
文献类型:
--
作者:
Zhao S;Chen W;Li W;Yu W;Li S;Rao T;Ruan Y;Zhou X;Liu C;Qi Y;Cheng F
Renal ischaemia/reperfusion (I/R) injury may induce kidney damage and dysfunction, in which oxidative stress and apoptosis play important roles. Long noncoding RNAs (lncRNAs) and microRNAs (miRNAs) are reported to be closely related to renal I/R, but the specific molecular mechanism is still unclear. The purpose of this research was to explore the regulatory effect of lncRNA TUG1 on oxidative stress and apoptosis in renal I/R injury. This research revealed that in renal I/R injury and hypoxia/reperfusion (H/R) injury in vitro, the expression level of lncRNA TUG1 was upregulated, and oxidative stress levels and apoptosis levels were negatively correlated with the expression level of lncRNA TUG1. Using bioinformatics databases such as TargetScan and microRNA.org, microRNA‐144‐3p (miR‐144‐3p) was predicted to be involved in the association between lncRNA TUG1 and Nrf2. This study confirmed that the level of miR‐144‐3p was significantly reduced following renal I/R injury and H/R injury in vitro, and miR‐144‐3p was determined to target Nrf2 and inhibit its expression. In addition, lncRNA TUG1 can reduce the inhibitory effect of miR‐144‐3p on Nrf2 by sponging miR‐144‐3p. In summary, our research shows that lncRNA TUG1 regulates oxidative stress and apoptosis during renal I/R injury through the miR‐144‐3p/Nrf2 axis, which may be a new treatment target for renal I/R injury.
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影响因子:
15.1
作者:
Hoste, Eric A. J.;Clermont, Gilles;Kersten, Alexander;Venkataraman, Ramesh;Angus, Derek C.;De Bacquer, Dirk;Kellum, John A.
通讯作者:
Kellum, John A.
DOI:
10.3390/molecules22030436
发表时间:
2017-03-09
期刊:
Molecules (Basel, Switzerland)
影响因子:
--
作者:
Fuse Y;Kobayashi M
通讯作者:
Kobayashi M
影响因子:
10.5
作者:
Itoh, K;Wakabayashi, N;Yamamoto, M
通讯作者:
Yamamoto, M
影响因子:
5.1
作者:
Anzell AR;Maizy R;Przyklenk K;Sanderson TH
通讯作者:
Sanderson TH
影响因子:
11.4
作者:
Joo Choi R;Cheng MS;Shik Kim Y
通讯作者:
Shik Kim Y