Regulatory role of ncRNAs in pulmonary epithelial and endothelial barriers: Molecular therapy clues of influenza-induced acute lung injury
Regulatory role of ncRNAs in pulmonary epithelial and endothelial barriers: Molecular therapy clues of influenza-induced acute lung injury
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DOI：
10.1016/j.phrs.2022.106509
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发表时间：
2022-10-26
影响因子：
9.3
通讯作者：
Li，Yan
中科院分区：
文献类型：
--
作者：
Zhang，Yi;Yang，Juan;Li，Yan
甲型流感病毒在全球范围内广泛传播，每年都会导致大量感染和急性肺损伤（ALI）死亡。肺泡上皮和微血管内皮细胞屏障功能的破坏和损害是流感病毒感染引起的ALI和急性呼吸窘迫综合征的关键诱发因素。非编码核糖核酸（noncoding ribonucleic acids，ncRNA）虽然不编码宿主细胞中的蛋白质，但具有蛋白质调控和信号转导的能力。此外，研究表明，ncRNA在流感病毒感染后显著且差异地表达，并且这些ncRNA在流感病毒感染的发病机制中起重要作用。通过分析最近发表的文献，我们发现ncRNA可以通过不同的方式调节肺泡上皮和微血管内皮细胞屏障功能，包括影响宿主细胞的先天性和获得性免疫反应，影响细胞凋亡和自噬，调节紧密连接和粘附连接等。本文综述了这些ncRNA的作用和调控机制，并讨论了这些ncRNA对肺上皮和内皮细胞屏障的影响。此外，通过整理和分析现有的研究数据，我们提出了将这些ncRNA用于治疗流感病例中的ALI的可能性，从而减轻肺上皮和内皮细胞屏障的通透性。最后，对今后的研究和发展前景进行了展望。基于ncRNA的靶向治疗和药物研究将为流感相关性ALI的分子治疗提供重要的方向。
Influenza A virus is globally widespread, causing a large number of infections and deaths due to acute lung injury (ALI) every year. The destruction and impairment of alveolar epithelial and microvascular endothelial cell barrier functions are the key inducers of ALI and acute respiratory distress syndrome caused by influenza virus infection. Although noncoding ribonucleic acids (ncRNAs) do not encode proteins in host cells, they possess the ability of protein regulation and signal transduction. Moreover, studies have shown that ncRNAs are significantly and differentially expressed following influenza virus infection, and these ncRNAs play vital roles in the pathogenesis of influenza virus infection. By analyzing the recently published literature, we found that ncRNA could regulate alveolar epithelial and microvascular endothelial cell barrier functions in different ways, which include influencing the innate and acquired immune responses of host cells, affecting apoptosis and autophagy, regulating tight and adherent junctions, etc. In the present paper, we reviewed the roles and regulatory mechanisms of these ncRNAs and discussed the effects of these ncRNAs on pulmonary epithelial and endothelial cell barriers. Further, by sorting and analyzing available research data, we proposed the possibility of applying these ncRNAs for treating ALI in influenza cases, thereby alleviating the permeability of pulmonary epithelial and endothelial cell barriers. Moreover, we discussed future research and development prospects. Our review suggests that targeted therapy and drug research based on ncRNAs would provide an important direction for the molecular therapy of influenza-induced ALI.