慢性阻塞性肺病
氧化应激
发病机制
医学
抗氧化剂
吸入
氧化磷酸化
免疫学
内科学
麻醉
化学
生物化学
作者
Francesco Nucera,Sharon Mumby,Keshav Raj Paudel,Vivek Dharwal,Antonino Di Stefano,Vincenzo Casolaro,Philip M. Hansbro,Ian M. Adcock,Gaetano Caramori
出处
期刊:Minerva Medica
[Edizioni Minerva Medica]
日期:2022-07-01
卷期号:113 (3)
被引量:24
标识
DOI:10.23736/s0026-4806.22.07972-1
摘要
Chronic inhalation of cigarette smoke is a prominent cause of chronic obstructive pulmonary disease (COPD) and provides an important source of exogenous oxidants. In addition, several inflammatory and structural cells are a source of endogenous oxidants in the lower airways of COPD patients, even in former smokers. This suggests that oxidants play a key role in the pathogenesis of COPD. This oxidative stress is counterbalanced by the protective effects of the various endogenous antioxidant defenses of the lower airways. A large amount of data from animal models and patients with COPD have shown that both the stable phase of the disease, and during exacerbations, have increased oxidative stress in the lower airways compared with age-matched smokers with normal lung function. Thus, counteracting the increased oxidative stress may produce clinical benefits in COPD patients. Smoking cessation is currently the most effective treatment of COPD patients and reduces oxidative stress in the lower airways. In addition, many drugs used to treat COPD have some antioxidant effects, however, it is still unclear if their clinical efficacy is related to pharmacological modulation of the oxidant/antioxidant balance. Several new antioxidant compounds are in development for the treatment of COPD.
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