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微小RNA在远程后适应诱导的中风保护中的新作用

Emerging Role of microRNAs in Stroke Protection Elicited by Remote Postconditioning.

作者信息

Pignataro Giuseppe

机构信息

Division of Pharmacology, Department of Neuroscience, School of Medicine, "Federico II" University of Naples, Naples, Italy.

出版信息

Front Neurol. 2021 Oct 21;12:748709. doi: 10.3389/fneur.2021.748709. eCollection 2021.

DOI:10.3389/fneur.2021.748709
PMID:34744984
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8567963/
Abstract

Remote ischemic conditioning (RIC) represents an innovative and attractive neuroprotective approach in brain ischemia. The purpose of this intervention is to activate endogenous tolerance mechanisms by inflicting a subliminal ischemia injury to the limbs, or to another "remote" region, leading to a protective systemic response against ischemic brain injury. Among the multiple candidates that have been proposed as putative mediators of the protective effect generated by the subthreshold peripheral ischemic insult, it has been hypothesized that microRNAs may play a vital role in the infarct-sparing effect of RIC. The effect of miRNAs can be exploited at different levels: (1) as transducers of protective messages to the brain or (2) as effectors of brain protection. The purpose of the present review is to summarize the most recent evidence supporting the involvement of microRNAs in brain protection elicited by remote conditioning, highlighting potential and pitfalls in their exploitation as diagnostic and therapeutic tools. The understanding of these processes could help provide light on the molecular pathways involved in brain protection for the future development of miRNA-based theranostic agents in stroke.

摘要

远程缺血预处理(RIC)是脑缺血领域一种创新且有吸引力的神经保护方法。这种干预的目的是通过对肢体或另一个“远程”区域施加阈下缺血损伤,激活内源性耐受机制,从而引发针对缺血性脑损伤的全身性保护反应。在众多被认为是阈下外周缺血损伤产生保护作用的潜在介质的候选分子中,有人推测微小RNA(microRNAs)可能在RIC的梗死灶保护效应中发挥重要作用。微小RNA的作用可在不同层面加以利用:(1)作为向大脑传递保护信息的转导分子,或(2)作为脑保护的效应分子。本综述的目的是总结支持微小RNA参与远程预处理诱导的脑保护作用的最新证据,突出将其用作诊断和治疗工具的潜力与问题。对这些过程的理解有助于为基于微小RNA的中风诊疗试剂的未来发展,阐明脑保护所涉及的分子途径。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9526/8567963/3d09b4184d63/fneur-12-748709-g0001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9526/8567963/3d09b4184d63/fneur-12-748709-g0001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9526/8567963/3d09b4184d63/fneur-12-748709-g0001.jpg

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The hypoxia sensitive metal transcription factor MTF-1 activates NCX1 brain promoter and participates in remote postconditioning neuroprotection in stroke.
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