From 2b173cb0a27557b17c9b8769dc0fe5afaa734ef8 Mon Sep 17 00:00:00 2001
From: wangjinlei <751475802@qq.com>
Date: Wed, 11 Feb 2026 16:53:58 +0800
Subject: [PATCH] 1

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 article_3113.tex | 1 +
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 \section{\textit{\textbf{Pathogenesis of COPD}}}
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 COPD is a progressive respiratory condition defined by significant airflow limitation, mucus overproduction, chronic bronchitis, emphysema, or damage to the alveolar septal walls. These manifestations lead to symptoms such as wheezing, coughing, and dyspnea, which can result in acute exacerbations, hospitalisation, and even death \parencite{ref_132735}.\par
 CS, pathogens, and various environmental exposures are significant external risk factors contributing to the development of COPD; notably, the removal of these risk factors has the potential to halt the pathological progression of the disease \textcolor[HTML]{0082AA}{[4, 15]}. Other factors, including genetics, gender, occupation, airway hyperresponsiveness, lung growth and development, and infections, also significantly contribute to the pathogenesis of COPD \parencite{ref_132735,ref_132736,ref_132737}. COPD is characterised by persistent inflammation and fibrosis of the small airways and the deterioration of lung parenchyma, also known as emphysema \textcolor[HTML]{0082AA}{[18, 19]}. COPD is complicatedly regulated by various biological mechanisms and their crosstalk, including oxidative stress, inflammation, ECM homeostasis, apoptosis, pyroptosis, and mucous cell hyperplasia \textcolor[HTML]{0082AA}{[7, 20-24]}. Among these, the regulation mechanism of oxidative stress and inflammation has attracted much attention in the field of COPD research and drug discovery, and airway remodelling and fibrosis are critical pathological features of late-stage COPD.\par
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