Suppr超能文献

脑缺血再灌注损伤后 miRNA 失调的原因和后果。

Causes and Consequences of MicroRNA Dysregulation Following Cerebral Ischemia-Reperfusion Injury.

机构信息

Medical Toxicology Research Center, Faculty of Medicine, Mashhad University of Medical Sciences, Mashhad, Iran.

Department of Neuroscience, Faculty of Medicine, Mashhad University of Medical Sciences, Mashhad, Iran.

出版信息

CNS Neurol Disord Drug Targets. 2019;18(3):212-221. doi: 10.2174/1871527318666190204104629.

Abstract

Stroke continues to be a major cause of death and disability worldwide. In this respect, the most important mechanisms underlying stroke pathophysiology are inflammatory pathways, oxidative stress, as well as apoptosis. Accordingly, miRNAs are considered as non-coding endogenous RNA molecules interacting with their target mRNAs to inhibit mRNA translation or reduce its transcription. Studies in this domain have similarly shown that miRNAs are strongly associated with coronary artery disease and correspondingly contributed to the brain ischemia molecular processes. To retrieve articles related to the study subject, i.e. the role of miRNAs involved in inflammatory pathways, oxidative stress, and apoptosis in stroke from the databases of Web of Science, PubMed (NLM), Open Access Journals, LISTA (EBSCO), and Google Scholar; keywords including cerebral ischemia, microRNA (miRNA), inflammatory pathway, oxidative stress, along with apoptosis were used. It was consequently inferred that, miRNAs could be employed as potential biomarkers for diagnosis and prognosis, as well as therapeutic goals of cerebral ischemia.

摘要

中风仍然是全世界范围内主要的死亡和残疾原因。在这方面,中风病理生理学的最重要机制是炎症途径、氧化应激以及细胞凋亡。相应地,miRNA 被认为是与靶 mRNA 相互作用以抑制 mRNA 翻译或减少其转录的非编码内源性 RNA 分子。该领域的研究同样表明,miRNA 与冠状动脉疾病密切相关,并相应地参与了脑缺血的分子过程。为了从 Web of Science、PubMed(NLM)、开放获取期刊、LISTA(EBSCO)和 Google Scholar 等数据库中检索与研究主题(即参与中风炎症途径、氧化应激和细胞凋亡的 miRNA 的作用)相关的文章,使用了包括脑缺血、microRNA(miRNA)、炎症途径、氧化应激和细胞凋亡在内的关键词。因此可以推断,miRNA 可以用作脑缺血的潜在诊断和预后生物标志物以及治疗靶点。

文献AI研究员

20分钟写一篇综述,助力文献阅读效率提升50倍。

立即体验

用中文搜PubMed

大模型驱动的PubMed中文搜索引擎

马上搜索

文档翻译

学术文献翻译模型,支持多种主流文档格式。

立即体验