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陆璐, 施爱民, 刘起展. 细胞外囊泡在吸烟所致慢性阻塞性肺病中作用及其机制研究进展[J]. 中国公共卫生, 2023, 39(3): 400-404. DOI: 10.11847/zgggws1139677
引用本文: 陆璐, 施爱民, 刘起展. 细胞外囊泡在吸烟所致慢性阻塞性肺病中作用及其机制研究进展[J]. 中国公共卫生, 2023, 39(3): 400-404. DOI: 10.11847/zgggws1139677
LU Lu, SHI Ai-min, LIU Qi-zhan. Role and mechanism of extracellular vesicles in smoking-induced chronic obstructive pulmonary disease: a review on research progress[J]. Chinese Journal of Public Health, 2023, 39(3): 400-404. DOI: 10.11847/zgggws1139677
Citation: LU Lu, SHI Ai-min, LIU Qi-zhan. Role and mechanism of extracellular vesicles in smoking-induced chronic obstructive pulmonary disease: a review on research progress[J]. Chinese Journal of Public Health, 2023, 39(3): 400-404. DOI: 10.11847/zgggws1139677

细胞外囊泡在吸烟所致慢性阻塞性肺病中作用及其机制研究进展

Role and mechanism of extracellular vesicles in smoking-induced chronic obstructive pulmonary disease: a review on research progress

  • 摘要: 慢性阻塞性肺病(chronic obstructive pulmonary disease, COPD)是一种复杂的异质性呼吸系统疾病,其主要是因长期吸入有害颗粒引起的肺功能和肺结构的改变。香烟烟雾(cigarette smoke, CS)是COPD的主要危险因素,其引起的炎症、细胞应激和组织破坏在COPD中发挥关键作用。细胞外囊泡(extracellular vesicles, EVs)为一种具有功能活性的纳米级膜结合囊泡,近年来因其在许多疾病诊断和治疗中发挥重要作用而受到越来越多的关注,但其在吸烟所致COPD中的作用及其机制的研究仍处于起步阶段,为此本文对EVs在CS所致COPD中的作用及其机制的国内外研究作一概述。

     

    Abstract: Chronic obstructive pulmonary disease (COPD) is a complex, heterogeneous respiratory disease that is characterized by functional and structural alterations mainly caused by long - term inhalation of harmful particles. Cigarette smoke (CS) is a major risk factor for COPD. Inflammation, cellular stress, and tissue damage caused by cigarette smoke play key roles in COPD progression. Extracellular vesicles (EVs) are functional nanoscale membrane - bound vesicles. Recently, EVs have attracted more and more attention due to their roles in the diagnosis and treatment of many diseases. However, the research on the roles and mechanism of EVs in smoking - induced COPD is still in its infancy. In this paper, we provided an overview of national and international research on the roles and mechanisms of EVs in the pathogenesis of CS - induced COPD.

     

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