The role of microRNAs involved in the disorder of blood-brain barrier in the pathogenesis of multiple sclerosis

(2023) The role of microRNAs involved in the disorder of blood-brain barrier in the pathogenesis of multiple sclerosis. Frontiers in Immunology. p. 16. ISSN 1664-3224

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Abstract

miRNAs are involved in various vital processes, including cell growth, development, apoptosis, cellular differentiation, and pathological cellular activities. Circulating miRNAs can be detected in various body fluids including serum, plasma, saliva, and urine. It is worth mentioning that miRNAs remain stable in the circulation in biological fluids and are released from membrane-bound vesicles called exosomes, which protect them from RNase activity. It has been shown that miRNAs regulate blood-brain barrier integrity by targeting both tight junction and adherens junction molecules and can also influence the expression of inflammatory cytokines. Some recent studies have examined the impact of certain commonly used drugs in Multiple Sclerosis on miRNA levels. In this review, we will focus on the recent findings on the role of miRNAs in multiple sclerosis, including their role in the cause of MS and molecular mechanisms of the disease, utilizing miRNAs as diagnostic and clinical biomarkers, using miRNAs as a therapeutic modality or target for Multiple Sclerosis and drug responses in patients, elucidating their importance as prognosticators of disease progression, and highlighting their potential as a future treatment for MS.

Item Type: Article
Keywords: miRNAs autoimmune multiple sclerosis exosomes therapeutic advances central-nervous-system circulating micrornas th17 differentiation peripheral-blood noncoding rnas emerging role expression biomarkers disease mirnas Immunology
Page Range: p. 16
Journal or Publication Title: Frontiers in Immunology
Journal Index: ISI
Volume: 14
Identification Number: https://doi.org/10.3389/fimmu.2023.1281567
ISSN: 1664-3224
Depositing User: خانم ناهید ضیائی
URI: http://eprints.mui.ac.ir/id/eprint/26046

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