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长链非编码 RNA SNHG14 通过调节 miR-93 在脓毒症诱导的急性肾损伤中发挥作用。

lncRNA SNHG14 Plays a Role in Sepsis-Induced Acute Kidney Injury by Regulating miR-93.

机构信息

Department of Intensive Care Unit, Henan Provincial People's Hospital, Zhengzhou, Henan, China.

Department of Intensive Care Unit, Zhongnan Hospital of Wuhan University, Wuhan, Hubei, China.

出版信息

Mediators Inflamm. 2021 Jan 6;2021:5318369. doi: 10.1155/2021/5318369. eCollection 2021.

Abstract

Acute kidney injury (AKI) is a common organ injury in sepsis, which leads to poor prognosis. Long noncoding RNA (lncRNA) small nucleolus RNA host gene 14 (SNHG14) was recognized to induce cell injury in LPS-induced acute lung injury and Parkinson's disease. We want to investigate the functions and mechanisms of SNHG14 in sepsis-induced AKI. Increased expression of SNHG14 was observed in LPS-induced HK-2 cells, and this was due to the activation of the TLR4/NF-B pathway. In vitro studies showed that SNHG14 was involved in the oxidative stress, inflammation, and apoptosis of LPS-induced HK-2 cells. Further investigations confirmed that SNHG14 exerted the functions via miR-93 which could regulate the activation of NF-B and STAT3 signaling by targeting IRAK4 and IL-6R. We also found that silencing SNHG14 also alleviated cellular injury processes of IL-1 and IL-6 in HK-2 cells via miR-93. We demonstrate that SNHG14 accelerates cellular injury in sepsis-induced AKI by activating IRAK4/NF-B and IL-6R/STAT3 signaling via miR-93.

摘要

急性肾损伤(AKI)是脓毒症中常见的器官损伤,导致预后不良。长链非编码 RNA(lncRNA)小核仁 RNA 宿主基因 14(SNHG14)被认为在 LPS 诱导的急性肺损伤和帕金森病中诱导细胞损伤。我们想研究 SNHG14 在脓毒症诱导的 AKI 中的作用和机制。在 LPS 诱导的 HK-2 细胞中观察到 SNHG14 的表达增加,这是由于 TLR4/NF-B 途径的激活。体外研究表明,SNHG14 参与 LPS 诱导的 HK-2 细胞的氧化应激、炎症和细胞凋亡。进一步的研究证实,SNHG14 通过 miR-93 发挥作用,通过靶向 IRAK4 和 IL-6R 来调节 NF-B 和 STAT3 信号的激活。我们还发现,沉默 SNHG14 还通过 miR-93 减轻 HK-2 细胞中 IL-1 和 IL-6 的细胞损伤过程。我们证明,SNHG14 通过 miR-93 激活 IRAK4/NF-B 和 IL-6R/STAT3 信号,加速脓毒症诱导的 AKI 中的细胞损伤。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4fcb/7806393/bcba0a979416/MI2021-5318369.001.jpg

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