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理解端粒磨损和表观遗传特征在 COVID-19 严重程度中的作用。

Understanding the role of telomere attrition and epigenetic signatures in COVID-19 severity.

机构信息

Immunology Research Center, Tabriz University of Medical Sciences, Tabriz, Iran.

Neurosciences Research center, Aging Research Institute, Tabriz University of Medical Sciences, Tabriz, Iran.

出版信息

Gene. 2022 Feb 15;811:146069. doi: 10.1016/j.gene.2021.146069. Epub 2021 Nov 27.

DOI:10.1016/j.gene.2021.146069
PMID:34848322
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8634871/
Abstract

Within the past several decades, the emergence and spread of infectious diseases with pandemic potential have endangered human lives. Coronavirus disease 2019 (COVID-19) outbreak represents an unprecedented threat for all health systems worldwide. The clinical spectrum of COVID-19 is highly heterogeneous, ranging from asymptomatic and mild upper respiratory tract illness to severe interstitial pneumonia with respiratory failure and even death. Highly age-dependent patterns of immune response potentially explain the higher rates of the severe forms of COVID-19 in elderly patients. However, genetic and epigenetic architecture can influence multiple biological processes during the lifespan, therefore as far as our knowledge shows, vulnerability to viral infection concerning telomere length and epigenetic signature is not a new idea. This review aims is to summarize the current understanding of the role of telomere length and epigenetic mechanisms on the severity of COVID-19. The current knowledge highlights the significant association between the shorter telomere length and the higher risk of developing severe COVID-19. Differential DNA methylation patterns and miRNA expression profiles imply that these hallmarks can play a pivotal role in COVID- 19 pathogenesis. Understanding the causes of inter-individual variations in COVID-19 outcomes could provide clues to the development of the personalized therapeutic intervention.

摘要

在过去几十年中,具有大流行潜力的传染病的出现和传播危及了人类的生命。2019 年冠状病毒病(COVID-19)的爆发对全球所有卫生系统构成了前所未有的威胁。COVID-19 的临床谱高度异质,从无症状和轻度上呼吸道疾病到严重的间质性肺炎伴呼吸衰竭甚至死亡。高度依赖年龄的免疫反应模式可能解释了老年患者 COVID-19 严重形式的更高发病率。然而,遗传和表观遗传结构可以在整个生命过程中影响多个生物学过程,因此就我们目前的知识而言,关于端粒长度和表观遗传特征与病毒感染易感性的问题并不是一个新观点。这篇综述旨在总结目前关于端粒长度和表观遗传机制对 COVID-19 严重程度的作用的认识。目前的知识强调了端粒较短与发生严重 COVID-19 的风险增加之间的显著关联。不同的 DNA 甲基化模式和 miRNA 表达谱表明,这些特征标志物可以在 COVID-19 的发病机制中发挥关键作用。了解 COVID-19 结局的个体间差异的原因可能为个性化治疗干预的发展提供线索。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/378a/8634871/0360b4be92ff/gr1_lrg.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/378a/8634871/0360b4be92ff/gr1_lrg.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/378a/8634871/0360b4be92ff/gr1_lrg.jpg

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