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微小RNA对氧化应激诱导的细胞衰老的调控

MicroRNA Regulation of Oxidative Stress-Induced Cellular Senescence.

作者信息

Bu Huaije, Wedel Sophia, Cavinato Maria, Jansen-Dürr Pidder

机构信息

Institute for Biomedical Aging Research and Center for Molecular Biosciences Innsbruck (CMBI), Universität Innsbruck, Innsbruck, Austria.

出版信息

Oxid Med Cell Longev. 2017;2017:2398696. doi: 10.1155/2017/2398696. Epub 2017 May 16.

DOI:10.1155/2017/2398696
PMID:28593022
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5448073/
Abstract

Aging is a time-related process of functional deterioration at cellular, tissue, organelle, and organismal level that ultimately brings life to end. Cellular senescence, a state of permanent cell growth arrest in response to cellular stress, is believed to be the driver of the aging process and age-related disorders. The free radical theory of aging, referred to as oxidative stress (OS) theory below, is one of the most studied aging promoting mechanisms. In addition, genetics and epigenetics also play large roles in accelerating and/or delaying the onset of aging and aging-related diseases. Among various epigenetic events, microRNAs (miRNAs) turned out to be important players in controlling OS, aging, and cellular senescence. miRNAs can generate rapid and reversible responses and, therefore, are ideal players for mediating an adaptive response against stress through their capacity to fine-tune gene expression. However, the importance of miRNAs in regulating OS in the context of aging and cellular senescence is largely unknown. The purpose of our article is to highlight recent advancements in the regulatory role of miRNAs in OS-induced cellular senescence.

摘要

衰老指的是在细胞、组织、细胞器及机体水平上与时间相关的功能衰退过程,最终会导致生命终结。细胞衰老,即细胞在应对细胞应激时进入永久性生长停滞的状态,被认为是衰老过程及与衰老相关疾病的驱动因素。衰老的自由基理论,以下简称为氧化应激(OS)理论,是研究最多的衰老促进机制之一。此外,遗传学和表观遗传学在加速和/或延缓衰老及衰老相关疾病的发生方面也发挥着重要作用。在各种表观遗传事件中,微小RNA(miRNA)已被证明是控制氧化应激、衰老和细胞衰老的重要因素。miRNA能够产生快速且可逆的反应,因此,凭借其微调基因表达的能力,是介导应激适应性反应的理想因素。然而,在衰老和细胞衰老背景下,miRNA在调节氧化应激中的重要性在很大程度上尚不清楚。我们这篇文章的目的是强调miRNA在氧化应激诱导的细胞衰老中的调节作用方面的最新进展。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bcc6/5448073/194fdfd80d94/OMCL2017-2398696.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bcc6/5448073/f240773901a0/OMCL2017-2398696.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bcc6/5448073/f2d079ab5325/OMCL2017-2398696.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bcc6/5448073/194fdfd80d94/OMCL2017-2398696.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bcc6/5448073/f240773901a0/OMCL2017-2398696.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bcc6/5448073/f2d079ab5325/OMCL2017-2398696.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bcc6/5448073/194fdfd80d94/OMCL2017-2398696.003.jpg

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