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[慢性阻塞性肺疾病中的氧化应激与基因多态性]

[Oxidative stress and genetic polymorphism in COPD].

作者信息

Dalsgarô Oli Jacob, Vestbo Jørgen

机构信息

Lungemedicinsk klinik 223/klinisk forskningsenhed 136, H:S Hvidovre Hospital, DK-2650 Hvidovre.

出版信息

Ugeskr Laeger. 2002 Aug 26;164(35):4056-61.

Abstract

Chronic obstructive pulmonary disease (COPD) is characterised by progressive diminution of pulmonary function with minimal reversibility. The initially organ-related symptoms gradually involve secondary organs and end-stage COPD can be considered a systemic disease. The most important cause of COPD is tobacco smoking. In recent years there has been increasing focus on the pathophysiological events leading to COPD, and oxidative stress has been suggested as one of the major pathophysiological factors. Clinical studies indicate a causal association between tobacco smoking, oxidative stress, increased inflammatory response, and destruction of lung parenchyma. This article reviews the clinical literature on oxidative stress as a pre-inflammatory state, leading to COPD in susceptible smokers.

摘要

慢性阻塞性肺疾病(COPD)的特征是肺功能进行性减退且可逆性极小。最初与器官相关的症状逐渐累及次要器官,终末期COPD可被视为一种全身性疾病。COPD最重要的病因是吸烟。近年来,人们越来越关注导致COPD的病理生理过程,氧化应激被认为是主要的病理生理因素之一。临床研究表明吸烟、氧化应激、炎症反应增加与肺实质破坏之间存在因果关系。本文综述了关于氧化应激作为一种炎症前状态导致易感吸烟者患COPD的临床文献。

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