Suppr超能文献

miR-155 作为多发性硬化症发病机制的重要调节因子。综述。

miR-155 as an Important Regulator of Multiple Sclerosis Pathogenesis. A Review.

机构信息

Department of General Biochemistry, Faculty of Biology and Environmental Protection, University of Lodz, Pomorska 141/143, 90-236 Lodz, Poland.

Department of Neurological Rehabilitation, Medical University of Lodz, Milionowa 14, 93-113 Lodz, Poland.

出版信息

Int J Mol Sci. 2021 Apr 21;22(9):4332. doi: 10.3390/ijms22094332.

Abstract

Multiple sclerosis (MS) is a chronic, immune-mediated disease and the leading cause of disability among young adults. MicroRNAs (miRNAs) are involved in the post-transcriptional regulation of gene expression. Of them, miR-155 is a crucial regulator of inflammation and plays a role in modulating the autoimmune response in MS. miR-155 is involved in blood-brain barrier (BBB) disruption via down-regulation of key junctional proteins under inflammatory conditions. It drives demyelination processes by contributing to, e.g., microglial activation, polarization of astrocytes, and down-regulation of CD47 protein and affecting crucial transcription factors. miR-155 has a huge impact on the development of neuropathic pain and indirectly influences a regulatory T (Treg) cell differentiation involved in the alleviation of pain hypersensitivity. This review also focused on neuropsychiatric symptoms appearing as a result of disease-associated stressors, brain atrophy, and pro-inflammatory factors. Recent studies revealed the role of miR-155 in regulating anxiety, stress, inflammation in the hippocampus, and treatment-resistant depression. Inhibition of miR-155 expression was demonstrated to be effective in preventing processes involved in the pathophysiology of MS. This review aimed to support the better understanding the great role of miR-155 dysregulation in various aspects of MS pathophysiology and highlight future perspectives for this molecule.

摘要

多发性硬化症(MS)是一种慢性、免疫介导的疾病,是年轻人残疾的主要原因。微小 RNA(miRNA)参与基因表达的转录后调控。其中,miR-155 是炎症的关键调节因子,在调节 MS 中的自身免疫反应中发挥作用。miR-155 通过下调炎症条件下关键连接蛋白来参与血脑屏障(BBB)的破坏。它通过促进小胶质细胞激活、星形胶质细胞极化和下调 CD47 蛋白以及影响关键转录因子来驱动脱髓鞘过程。miR-155 对神经病理性疼痛的发展有巨大影响,并间接影响参与缓解疼痛过敏的调节性 T(Treg)细胞分化。本综述还重点关注了由于疾病相关应激、脑萎缩和促炎因子引起的神经精神症状。最近的研究揭示了 miR-155 在调节海马体中的焦虑、应激、炎症以及治疗抵抗性抑郁症中的作用。抑制 miR-155 的表达被证明在预防 MS 病理生理学中涉及的过程方面是有效的。本综述旨在支持更好地理解 miR-155 失调在 MS 病理生理学各个方面的重要作用,并强调该分子的未来前景。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/318b/8122504/7bfbd1d3b8b7/ijms-22-04332-g001.jpg

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