慢性阻塞性肺病病理特征的新见解:关注氧化应激和有丝分裂

Jiameng Gao, Yao Shen, Zhihong Chen
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摘要

慢性气道阻塞性肺病(COPD)是一种可预防和治愈的疾病,其特点是持续的气流受限。它以慢性支气管炎和/或肺气肿为特征,病因与吸烟、感染因素等多种因素有关。慢性阻塞性肺病的发病机制复杂,容易频繁加重,急性加重期的预后往往较差。作为先天性免疫系统的重要组成部分,肺巨噬细胞对慢性阻塞性肺病的发病和进展有重要影响。当巨噬细胞线粒体功能失调时,巨噬细胞的许多功能(如吞噬、细胞因子分泌、趋化等)都会发生变化。本文旨在描述慢性阻塞性肺病的三大病理特征(氧化应激失衡、巨噬细胞极化及线粒体膜电位[MMP]产生和线粒体自噬),详细描述线粒体自噬途径的机制及其与氧化应激和巨噬细胞极化的关系,并强调巨噬细胞线粒体活性氧(mROS)在慢性阻塞性肺病中的作用,以期为后续研究提供思路和方向。
本文章由计算机程序翻译,如有差异,请以英文原文为准。

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Novel insights into the pathological features of COPD: Focus on oxidative stress and mitophagy

Chronic airway obstructive pulmonary disease (COPD) is a preventable and curable disease characterised by persistent airflow limitation. It is characterised by chronic bronchitis and/or emphysema, and its aetiology is related to various factors such as smoking and infectious factors, and so forth. The pathogenesis is complex and prone to frequent exacerbations, and the prognosis of acute exacerbations of COPD is often poor. As a crucial component of the innate immune system, lung macrophages significantly influence the onset and progression of COPD. When macrophage mitochondria become dysfunctional, many macrophage functions (e.g., phagocytosis, cytokine secretion, chemotaxis, etc.) change. The aim of this paper is to describe the three major pathological features of COPD (oxidative stress imbalance, macrophage polarisation and mitochondrial membrane potential [MMP] production and mitochondrial autophagy), to describe in detail the mechanism of mitochondrial autophagy pathway and its association with oxidative stress and macrophage polarisation and to emphasise the role of macrophage mitochondrial reactive oxygen species (mROS) in COPD, with the aim of providing ideas and directions for subsequent studies.

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