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坏死性凋亡在慢性阻塞性肺疾病气流受限中的作用:聚焦于小气道疾病和肺气肿

Role of necroptosis in airflow limitation in chronic obstructive pulmonary disease: focus on small-airway disease and emphysema.

作者信息

Liu Chanjing, Li Peijun, Zheng Jiejiao, Wang Yingqi, Wu Weibing, Liu Xiaodan

机构信息

Department of Sports Rehabilitation, Shanghai University of Sport, Shanghai, People's Republic of China.

Department of Rehabilitation Medicine, Huadong Hospital, Shanghai, People's Republic of China.

出版信息

Cell Death Discov. 2022 Aug 16;8(1):363. doi: 10.1038/s41420-022-01154-7.

Abstract

Airflow limitation with intractable progressive mechanisms is the main disease feature of chronic obstructive pulmonary disease (COPD). The pathological process of airflow limitation in COPD involves necroptosis, a form of programmed necrotic cell death with pro-inflammatory properties. In this paper, the correlations of small-airway disease and emphysema with airflow limitation in COPD were firstly reviewed; then, based on this, the effects of necroptosis on small-airway disease and emphysema were analysed, and the possible mechanisms of necroptosis causing airflow limitation in COPD were explored. The results showed that airflow limitation is caused by a combination of small-airway disease and emphysema. In addition, toxic particulate matter stimulates epithelial cells to trigger necroptosis, and necroptosis promotes the expulsion of cell contents, the abnormal hyperplasia of pro-inflammatory mediators and the insufficient clearance of dead cells by macrophages; these processes, coupled with the interaction of necroptosis and oxidative stress, collectively result in small-airway disease and emphysema in COPD.

摘要

气流受限伴有难以控制的进行性机制是慢性阻塞性肺疾病(COPD)的主要疾病特征。COPD中气流受限的病理过程涉及坏死性凋亡,这是一种具有促炎特性的程序性坏死性细胞死亡形式。本文首先综述了小气道疾病和肺气肿与COPD气流受限的相关性;然后在此基础上,分析了坏死性凋亡对小气道疾病和肺气肿的影响,并探讨了坏死性凋亡导致COPD气流受限的可能机制。结果表明,气流受限是由小气道疾病和肺气肿共同引起的。此外,有毒颗粒物刺激上皮细胞引发坏死性凋亡,坏死性凋亡促进细胞内容物的排出、促炎介质的异常增生以及巨噬细胞对死亡细胞清除不足;这些过程,再加上坏死性凋亡与氧化应激的相互作用,共同导致了COPD中的小气道疾病和肺气肿。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a9e8/9381515/802140687470/41420_2022_1154_Fig1_HTML.jpg

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