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晚期糖基化终末产物受体及其配体高迁移率族蛋白 B1 在 COPD 发病机制中的作用。

Role of RAGE and its ligand HMGB1 in the development of COPD.

机构信息

Department of Respiratory and Critical Care Medicine, Liuzhou People's Hospital, LiuZhou, China.

Department of Respiratory and Critical Care Medicine, The First Affiliated Hospital of Guangxi Medical University, Nanning, China.

出版信息

Postgrad Med. 2022 Nov;134(8):763-775. doi: 10.1080/00325481.2022.2124087. Epub 2022 Sep 15.

DOI:10.1080/00325481.2022.2124087
PMID:36094155
Abstract

Smoking is a well-established risk factor for chronic obstructive pulmonary disease (COPD). Chronic lung inflammation continues even after smoking cessation and leads to COPD progression. To date, anti-inflammatory therapies are ineffective in improving pulmonary function and COPD symptoms, and new molecular targets are urgently needed to deal with this challenge. The receptor for advanced glycation end-products (RAGE) was shown to be relevant in COPD pathogenesis, since it is both a genetic determinant of low lung function and a determinant of COPD susceptibility. Moreover, RAGE is involved in the physiological response to cigarette smoke exposure. Since innate and acquired immunity plays an essential role in the development of chronic inflammation and emphysema in COPD, here we summarized the roles of RAGE and its ligand HMGB1 in COPD immunity.

摘要

吸烟是慢性阻塞性肺疾病(COPD)的一个既定危险因素。即使在戒烟后,慢性肺部炎症仍在继续,并导致 COPD 进展。迄今为止,抗炎疗法在改善肺功能和 COPD 症状方面效果不佳,因此迫切需要新的分子靶点来应对这一挑战。晚期糖基化终产物(RAGE)受体在 COPD 发病机制中具有相关性,因为它既是肺功能降低的遗传决定因素,也是 COPD 易感性的决定因素。此外,RAGE 参与了对香烟烟雾暴露的生理反应。由于先天和获得性免疫在 COPD 慢性炎症和肺气肿的发展中起着至关重要的作用,因此,在这里我们总结了 RAGE 及其配体 HMGB1 在 COPD 免疫中的作用。

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