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长非编码 RNA 在缺血性损伤中的功能作用研究进展(综述)。

An update on the functional roles of long non‑coding RNAs in ischemic injury (Review).

机构信息

School of Basic Medical Sciences, Shaoyang University, Shaoyang, Hunan 422000, P.R. China.

Department of Human Anatomy, School of Basic Medicine, Nanchang University, Nanchang, Jiangxi 330006, P.R. China.

出版信息

Int J Mol Med. 2022 Jul;50(1). doi: 10.3892/ijmm.2022.5147. Epub 2022 May 20.

DOI:10.3892/ijmm.2022.5147
PMID:35593308
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9170192/
Abstract

Ischemic injuries result from ischemia and hypoxia in cells. Tissues and organs receive an insufficient supply of nutrients and accumulate metabolic waste, which leads to the development of inflammation, fibrosis and a series of other issues. Ischemic injuries in the brain, heart, kidneys, lungs and other organs can cause severe adverse effects. Acute renal ischemia induces acute renal failure, heart ischemia induces myocardial infarction and cerebral ischemia induces cerebrovascular accidents, leading to loss of movement, consciousness and possibly, life‑threatening disabilities. Existing evidence suggests that long non‑coding RNAs (lncRNAs) are regulatory sequences involved in transcription, post‑transcription, epigenetic regulation and multiple physiological processes. lncRNAs have been shown to be differentially expressed following ischemic injury, with the severity of the ischemic injury being affected by the upregulation or downregulation of certain types of lncRNA. The present review article provides an extensive summary of the functional roles of lncRNAs in ischemic injury, with a focus on the brain, heart, kidneys and lungs. The present review mainly summarizes the functional roles of lncRNA MALAT1, lncRNA MEG3, lncRNA H19, lncRNA TUG1, lncRNA NEAT1, lncRNA AK139328 and lncRNA CAREL, among which lncRNA MALAT1, in particular, plays a crucial role in ischemic injury and is currently a hot research topic.

摘要

缺血性损伤是由细胞的缺血和缺氧引起的。组织和器官接收的营养物质供应不足,代谢废物堆积,导致炎症、纤维化和一系列其他问题的发展。脑、心、肾、肺等器官的缺血性损伤会导致严重的不良后果。急性肾缺血引起急性肾衰竭,心肌缺血引起心肌梗死,脑缺血引起脑血管意外,导致运动、意识丧失,甚至可能危及生命的残疾。现有证据表明,长链非编码 RNA(lncRNA)是参与转录、转录后、表观遗传调控和多种生理过程的调节序列。lncRNA 的表达在缺血性损伤后发生差异表达,某些类型的 lncRNA 的上调或下调会影响缺血性损伤的严重程度。本文综述了 lncRNA 在缺血性损伤中的功能作用,重点关注脑、心、肾和肺。本文主要总结了 lncRNA MALAT1、lncRNA MEG3、lncRNA H19、lncRNA TUG1、lncRNA NEAT1、lncRNA AK139328 和 lncRNA CAREL 的功能作用,其中 lncRNA MALAT1 在缺血性损伤中尤其发挥关键作用,是目前的热门研究课题。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6ac7/9170192/3bb34c886e7e/IJMM-50-01-05147-g01.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6ac7/9170192/7b2a68c5e479/IJMM-50-01-05147-g00.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6ac7/9170192/3bb34c886e7e/IJMM-50-01-05147-g01.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6ac7/9170192/7b2a68c5e479/IJMM-50-01-05147-g00.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6ac7/9170192/3bb34c886e7e/IJMM-50-01-05147-g01.jpg

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miR-204-5p is sponged by TUG1 to aggravate neuron damage induced by focal cerebral ischemia and reperfusion injury through upregulating COX2.TUG1可吸附miR-204-5p,通过上调COX2加重局灶性脑缺血再灌注损伤诱导的神经元损伤。
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LncRNAs and CircRNAs as Strategies against Pathological Conditions Caused by a Hypoxic/Anoxic State.长链非编码 RNA 和环状 RNA 作为应对缺氧/缺血状态引起的病理状况的策略。
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