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Physiology 21: 396-403, 2006; doi:10.1152/physiol.00027.2006
1548-9213/06 $8.00
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Physiology, Vol. 21, No. 6, 396-403, December 2006
© 2006 Int. Union Physiol. Sci./Am. Physiol. Soc.

REVIEW

Pulmonary Emphysema: When More is Less

David G. Morris1 and Dean Sheppard2

1 Respiratory Research, Roche Palo Alto, LLC, F. Hoffman-LaRoche, Ltd., Palo Alto; and
2 Department of Medicine, Division of Pulmonary and Critical Care Medicine, University of California-San Francisco, San Francisco, California Dave.Morris{at}Roche.com

Pulmonary emphysema results from the loss of intricate alveolar architecture and progressive simplification of small and highly effective gas-exchanging units into large, inefficient cyst-like spaces. Because of the loss of alveolar gas-exchanging units and the capillary bed within them, blood oxygen levels eventually fall and pressures within the pulmonary circulation rise. Recent insights from genetically manipulated mouse models have refined our understanding of the molecular events that prevent or promote the development of pulmonary emphysema. Capitalizing on an improved molecular understanding of emphysema with improved therapeutics has the potential to enhance both the survival and quality of life of patients with this common lung disease.






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