Molecular pathogenesis of emphysema

被引:199
作者
Taraseviciene-Stewart, Lairnute [1 ]
Voelkel, Norbert F. [1 ]
机构
[1] Univ Colorado, Hlth Sci Ctr, Div Pulm & Crit Care Med, Denver, CO 80202 USA
关键词
D O I
10.1172/JCI31811
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
Emphysema is one manifestation of a group of chronic, obstructive, and frequently progressive destructive lung diseases. Cigarette smoking and air pollution are the main causes of emphysema in humans, and cigarette smoking causes emphysema in rodents. This review examines the concept of a homeostatically active lung structure maintenance program that, when attacked by proteases and oxidants, leads to the loss of alveolar septal cells and airspace enlargement. inflammatory and noninflammatory mechanisms of disease pathogenesis, as well as the role of the innate and adaptive immune systems, are being explored in genetically altered animals and in exposure models of this disease. These recent scientific advances support a model whereby alveolar destruction resulting from a coalescence of mechanical forces, such as hyperinflation, and more recently recognized cellular and molecular events, including apoptosis, cellular senescence, and failed lung tissue repair, produces the clinically recognized syndrome of emphysema.
引用
收藏
页码:394 / 402
页数:9
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