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慢性阻塞性肺疾病的发病机制:从体内动物模型中获得的经验教训。

The pathogenesis of COPD: lessons learned from in vivo animal models.

作者信息

Fujita Masaki, Nakanishi Yoichi

机构信息

Research Institute for Diseases of the Chest, Graduate School of Medical Sciences, Kyushu University, Fukuoka, Japan.

出版信息

Med Sci Monit. 2007 Feb;13(2):RA19-24.

Abstract

Chronic obstructive pulmonary disease (COPD) is characterized by airflow limitations, that are not fully reversible. COPD is a major cause of chronic morbidity and mortality throughout the world. Tobacco smoking is a most important risk factor for the development of COPD. However, only 10 to 20% smokers develop clinically significant COPD. The detailed pathogenesis also remains to be elucidated. In vivo animal models provided some clues to help clarify the pathogenesis. Several important factors such as matrix metalloproteinases, apoptosis, protease-antiprotease imbalance, are considered to contribute to the development of COPD. In addition to these factors, chronic inflammation affects lung morphogenesis and causes several pathological involvements including COPD. In this article, we review the pathogenesis of COPD, while especially focusing on the recent advances and the effects of chronic inflammation using an in vivo animal model. This article aims at offering valuable information for both proceeding with COPD research as well as for developing a new medicines for the treatment of COPD.

摘要

慢性阻塞性肺疾病(COPD)的特征是气流受限,且这种受限不完全可逆。COPD是全球慢性发病和死亡的主要原因。吸烟是COPD发生的最重要风险因素。然而,只有10%至20%的吸烟者会发展为具有临床意义的COPD。其详细发病机制仍有待阐明。体内动物模型提供了一些有助于阐明发病机制的线索。诸如基质金属蛋白酶、细胞凋亡、蛋白酶-抗蛋白酶失衡等几个重要因素被认为与COPD的发生有关。除这些因素外,慢性炎症影响肺形态发生并导致包括COPD在内的多种病理改变。在本文中,我们综述了COPD的发病机制,尤其关注使用体内动物模型的最新进展以及慢性炎症的影响。本文旨在为推进COPD研究以及开发治疗COPD的新药提供有价值的信息。

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