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急性肾损伤中长链非编码RNA的最新进展

An Update of Long-Noncoding RNAs in Acute Kidney Injury.

作者信息

Yang Lina, Wang Bo, Ma Liang, Fu Ping

机构信息

Kidney Research Institute, Division of Nephrology, West China Hospital of Sichuan University, Chengdu, China.

出版信息

Front Physiol. 2022 Mar 8;13:849403. doi: 10.3389/fphys.2022.849403. eCollection 2022.

DOI:10.3389/fphys.2022.849403
PMID:35350698
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8957988/
Abstract

Acute kidney injury (AKI) is a global public health concern with high morbidity, mortality, and medical costs. Despite advances in medicine, effective therapeutic regimens for AKI remain limited. Long non-coding RNAs (lncRNAs) are a subtype of non-coding RNAs, which longer than 200 nucleotides and perform extremely diverse functions in biological processes. Recently, lncRNAs have emerged as promising biomarkers and key mediators to AKI. Meanwhile, existing research reveals that the aberrant expression of lncRNAs has been linked to major pathological processes in AKI, including the inflammatory response, cell proliferation, and apoptosis, forming the lncRNA/microRNA/target gene regulatory axis. Following a comprehensive and systematic search of the available literature, 87 relevant papers spanning the years 2005 to 2021 were identified. This review aims to provide and update an overview of lncRNAs in AKI, and further shed light on their potential utility as AKI biomarkers and therapeutic targets.

摘要

急性肾损伤(AKI)是一个全球性的公共卫生问题,具有高发病率、高死亡率和高昂的医疗成本。尽管医学取得了进展,但针对AKI的有效治疗方案仍然有限。长链非编码RNA(lncRNA)是非编码RNA的一个亚型,其长度超过200个核苷酸,在生物过程中发挥着极其多样的功能。最近,lncRNAs已成为AKI有前景的生物标志物和关键介质。同时,现有研究表明,lncRNAs的异常表达与AKI的主要病理过程有关,包括炎症反应、细胞增殖和凋亡,形成了lncRNA/微小RNA/靶基因调控轴。在对现有文献进行全面系统的检索后,共确定了87篇2005年至2021年期间的相关论文。本综述旨在提供并更新关于AKI中lncRNAs的概述,并进一步阐明它们作为AKI生物标志物和治疗靶点的潜在用途。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/12d8/8957988/e92cc6380f67/fphys-13-849403-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/12d8/8957988/a44b81923982/fphys-13-849403-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/12d8/8957988/e92cc6380f67/fphys-13-849403-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/12d8/8957988/a44b81923982/fphys-13-849403-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/12d8/8957988/e92cc6380f67/fphys-13-849403-g002.jpg

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本文引用的文献

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Kidney fibrosis: from mechanisms to therapeutic medicines.肾脏纤维化:从机制到治疗药物。
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