Role of non-coding RNAs and exosomal non-coding RNAs in vasculitis: A narrative review

被引：0

作者：

Tang, Xiuming ^{[1
]}

Guo, Jiajuan ^{[1
]}

Qi, Feng ^{[1
]}

Rezaei, Mohammad J. ^{[2
]}

机构：

[1] Department of Cardiology, The affiliated hospital to Changchun University of Chinise Medicine, Jilin, Changchun,130021, China

[2] Institute for Immunology and Immune Health, University of Pennsylvania Perelman School of Medicine, Philadelphia,PA, United States

来源：

International Journal of Biological Macromolecules | 2024年 / 261卷

关键词：

Blood vessels - Cell death - Diseases;

D O I：

暂无

中图分类号：

学科分类号：

摘要：

A category of very uncommon systemic inflammatory blood vessel illnesses known as vasculitides. The pathogenesis and etiology of vasculitis are still poorly known. Despite all of the progress made in understanding the genetics and causes behind vasculitis, there is still more to learn. Epigenetic dysregulation is a significant contributor to immune-mediated illnesses, and epigenetic aberrancies in vasculitis are becoming more widely acknowledged. Less than 2 % of the genome contains protein-encoding DNA. Studies have shown that a variety of RNAs originating from the non-coding genome exist. Long non-coding RNAs (lncRNAs), microRNAs (miRNAs), and circular RNAs (circRNAs) have attracted the most attention in recent years as they are becoming more and more important regulators of different biological processes, such as diseases of the veins. Extracellular vehicles (EVs) such as exosomes, are membrane-bound vesicular structures that break free either during programmed cell death, such as apoptosis, pyroptosis, and necroptosis or during cell activation. Exosomes may be involved in harmful ways in inflammation, procoagulation, autoimmune reactions, endothelial dysfunction/damage, intimal hyperplasia and angiogenesis, all of which may be significant in vasculitis. Herein, we summarized various non-coding RNAs that are involved in vasculitides pathogenesis. Moreover, we highlighted the role of exosomes in vasculitides. © 2024 Elsevier B.V.

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