Department of Microbiology, Immunology, and Inflammation, Temple University, Philadelphia, PA 19140, USA; Center for Inflammation and Lung Research, Temple University, Philadelphia, PA 19140, USA.
Department of Microbiology, Immunology, and Inflammation, Temple University, Philadelphia, PA 19140, USA; Center for Inflammation and Lung Research, Temple University, Philadelphia, PA 19140, USA; Department of Biomedical Education and Data Science, Temple University, Philadelphia, PA 19140, USA.
Biomed Pharmacother. 2021 Nov;143:112216. doi: 10.1016/j.biopha.2021.112216. Epub 2021 Sep 27.
Chronic obstructive pulmonary disease (COPD) is an inflammatory lung disease becoming one of the leading causes of mortality and morbidity globally. The significant risk factors for COPD are exposure to harmful particles such as cigarette smoke, biomass smoke, and air pollution. Pulmonary emphysema belongs to COPD and is characterized by a unique alveolar destruction pattern resulting in marked airspace enlargement. Alveolar type II (ATII) cells have stem cell potential; they proliferate and differentiate to alveolar type I cells to restore the epithelium after damage. Oxidative stress causes premature cell senescence that can contribute to emphysema development. MiRNAs regulate gene expression, are essential for maintaining ATII cell homeostasis, and their dysregulation contributes to this disease development. They also serve as biomarkers of lung diseases and potential therapeutics. In this review, we summarize recent findings on miRNAs' role in alveolar epithelial cells in emphysema.
慢性阻塞性肺疾病（COPD）是一种肺部炎症性疾病，已成为全球范围内导致死亡和发病的主要原因之一。COPD 的主要危险因素是接触有害颗粒，如香烟烟雾、生物质烟雾和空气污染。肺气肿属于 COPD，其特征是独特的肺泡破坏模式，导致明显的气腔扩大。肺泡 II 型（ATII）细胞具有干细胞潜能；它们增殖并分化为肺泡 I 型细胞，在损伤后修复上皮。氧化应激导致细胞过早衰老，这可能导致肺气肿的发展。miRNAs 调节基因表达，对维持 ATII 细胞的内稳态至关重要，其失调也会导致这种疾病的发展。它们还可以作为肺部疾病的生物标志物和潜在的治疗靶点。在这篇综述中，我们总结了最近关于 miRNAs 在肺气肿中肺泡上皮细胞作用的研究结果。
