Pathobiologic Mechanisms of Chronic Obstructive Pulmonary Disease

被引：74

作者：

Tam, Anthony ^{[1
]}

机构：

[1] Univ British Columbia, Dept Med, UBC James Hogg Res Ctr, Providence Heart & Lung Ctr, Vancouver, BC, Canada

来源：

MEDICAL CLINICS OF NORTH AMERICA | 2012年 / 96卷 / 04期

关键词：

Cigarette smoke; COPD; Pathobiologic mechanism; Inflammation; Immunity; NECROSIS-FACTOR-ALPHA; CIGARETTE-SMOKE EXPOSURE; SMALL-AIRWAY OBSTRUCTION; EPITHELIAL-CELLS; NEUTROPHIL ELASTASE; REGULATES MUCIN; MESSENGER-RNA; LUNG-FUNCTION; FEV1; DECLINE; GUINEA-PIGS;

D O I：

10.1016/j.mcna.2012.04.012

中图分类号：

R5 [内科学];

学科分类号：

1002 ; 100201 ;

摘要：

The pathogenesis of chronic obstructive pulmonary disease (COPD) is not fully known. However, it is now well accepted that inflammatory responses to external triggers, such as cigarette smoke and biomass fuel, are important in COPD progression. Protease-antiprotease balance, autoimmunity, mucus hypersecretion, airway wall remodeling, and chronic respiratory infections have all been implicated in disease pathogenesis. This article reviews these and other pathways that have been associated with COPD.

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页码：681 / +

页数：19

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