非编码RNA作为特发性肺纤维化和慢性阻塞性肺疾病中细胞衰老的调节因子
Non-coding RNAs as Regulators of Cellular Senescence in Idiopathic Pulmonary Fibrosis and Chronic Obstructive Pulmonary Disease.
作者信息
Omote Norihito, Sauler Maor
机构信息
Pulmonary, Critical Care and Sleep Medicine Section, Department of Internal Medicine, Yale University School of Medicine, New Haven, CT, United States.
出版信息
Front Med (Lausanne). 2020 Dec 23;7:603047. doi: 10.3389/fmed.2020.603047. eCollection 2020.
Abstract
Cellular senescence is a cell fate implicated in the pathogenesis of idiopathic pulmonary fibrosis (IPF) and chronic obstructive pulmonary disease (COPD). Cellular senescence occurs in response to cellular stressors such as oxidative stress, DNA damage, telomere shortening, and mitochondrial dysfunction. Whether these stresses induce cellular senescence or an alternative cell fate depends on the type and magnitude of cellular stress, but also on intrinsic factors regulating the cellular stress response. Non-coding RNAs, including both microRNAs and long non-coding RNAs, are key regulators of cellular stress responses and susceptibility to cellular senescence. In this review, we will discuss cellular mechanisms that contribute to senescence in IPF and COPD and highlight recent advances in our understanding of how these processes are influenced by non-coding RNAs. We will also discuss the potential therapeutic role for targeting non-coding RNAs to treat these chronic lung diseases.
摘要
细胞衰老与特发性肺纤维化（IPF）和慢性阻塞性肺疾病（COPD）的发病机制相关，是一种细胞命运。细胞衰老的发生是对氧化应激、DNA损伤、端粒缩短和线粒体功能障碍等细胞应激源的响应。这些应激是否会诱导细胞衰老或其他细胞命运，取决于细胞应激的类型和程度，也取决于调节细胞应激反应的内在因素。包括微小RNA和长链非编码RNA在内的非编码RNA是细胞应激反应和细胞衰老易感性的关键调节因子。在本综述中，我们将讨论导致IPF和COPD中细胞衰老的细胞机制，并强调我们对这些过程如何受非编码RNA影响的最新认识进展。我们还将讨论靶向非编码RNA治疗这些慢性肺病的潜在治疗作用。
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