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J Clin Invest. 2008 Feb;118(2):394-402. doi: 10.1172/JCI31811.

Molecular pathogenesis of emphysema.

Author information

1
Pulmonary and Critical Care Medicine Division, University of Colorado Health Sciences Center, Denver, Colorado, USA.

Abstract

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.

PMID:
18246188
PMCID:
PMC2214683
DOI:
10.1172/JCI31811
[Indexed for MEDLINE]
Free PMC Article

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