Pathogenesis of chronic obstructive pulmonary disease

被引：396

作者：

Tuder, Rubin M. ^{[1
]}

Petrache, Irina ^{[2
,3
]}

机构：

[1] Univ Colorado, Sch Med, Dept Med, Program Translat Lung Res,Div Pulm Sci & Crit Car, Denver, CO USA

[2] Indiana Univ, Dept Med, Div Pulm & Crit Care Med, Indianapolis, IN USA

[3] Indiana Univ, Richard L Roudebush Vet Affairs Med Ctr, Indianapolis, IN 46204 USA

来源：

JOURNAL OF CLINICAL INVESTIGATION | 2012年 / 122卷 / 08期

关键词：

SMOKE-INDUCED EMPHYSEMA; ENDOTHELIAL GROWTH-FACTOR; INDUCED LUNG INFLAMMATION; COPD-LIKE DISEASE; OXIDATIVE STRESS; ALVEOLAR MACROPHAGES; AIRWAY INFLAMMATION; CELL APOPTOSIS; ENHANCES SUSCEPTIBILITY; CONNECTIVE-TISSUE;

D O I：

10.1172/JCI60324

中图分类号：

R-3 [医学研究方法]; R3 [基础医学];

学科分类号：

1001 ;

摘要：

The current epidemic of chronic obstructive pulmonary disease (COPD) has produced a worldwide health care burden, approaching that imposed by transmittable infectious diseases. COPD is a multidimensional disease, with varied intermediate and clinical phenotypes. This Review discusses the pathogenesis of COPD, with particular focus on emphysema, based on the concept that pulmonary injury involves stages of initiation (by exposure to cigarette smoke, pollutants, and infectious agents), progression, and consolidation. Tissue damage entails complex interactions among oxidative stress, inflammation, extracellular matrix proteolysis, and. apoptotic and autophagic cell death. Lung damage by cigarette smoke ultimately leads to self-propagating processes, resulting in macromolecular and structural alterations features similar to those seen in aging.

引用

页码：2749 / 2755

页数：7

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