Proceedings of the American Thoracic Society Email Content Delivery
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
QUICK SEARCH:   [advanced]


     

The Proceedings of the American Thoracic Society 5:475-477 (2008)
© 2008 The American Thoracic Society
doi: 10.1513/pats.200708-126ET
This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Related articles in Proceedings of the American Thoracic Society
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrow reprints & permissions
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Sharafkhaneh, A.
Right arrow Articles by Kim, V.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Sharafkhaneh, A.
Right arrow Articles by Kim, V.

Pathogenesis of Emphysema

From the Bench to the Bedside

Amir Sharafkhaneh1, Nicola A. Hanania1 and Victor Kim2

1 Division of Pulmonary, Critical Care and Sleep Medicine, Baylor College of Medicine, and Michael E. DeBakey Veterans Affairs Medical Center, Houston, Texas; and 2 Division of Pulmonary and Critical Care Medicine, Temple University School of Medicine, Philadelphia, Pennsylvania

Correspondence and requests for reprints should be addressed to Amir Sharafkhaneh, M.D., F.C.C.P., Division of Pulmonary, Critical Care and Sleep Medicine, Michael E. DeBakey VAMC, Bldg 100 (111i), 2002 Holcombe Boulevard, Houston, TX 77030. E-mail: amirs{at}bcm.tmc.edu

ABSTRACT

Chronic obstructive pulmonary disease (COPD) is characterized physiologically by expiratory flow limitation and pathologically by alveolar destruction and enlargement and small and large airway inflammation and remodeling. An imbalance between protease and antiprotease activity in the lung is proposed as the major mechanism resulting in emphysema. The imbalance is mostly due to an increase in the numbers of alveolar macrophages and neutrophils. Emphysema can also develop from increased alveolar wall cell death and/or failure in alveolar wall maintenance. Chronic inflammation and increased oxidative stress contribute to increased destruction and/or impaired lung maintenance and repair. Genetic factors may play an important role in disease susceptibility because only a minority of smokers develops emphysema. Recent literature implicates surfactant instability, malnutrition, and alveolar cell apoptosis as possible etiologies. Identification of cellular and molecular mechanisms of COPD pathogenesis is an area of active, ongoing research that may help to determine therapeutic targets for emphysema.

Key Words: emphysema • apoptosis • protease–antiprotease balance • oxidative stress • hypoxemia


Related articles in Proceedings of the American Thoracic Society:

National Emphysema Treatment Trial State of the Art: Genetics of Emphysema
Craig P. Hersh, Dawn L. DeMeo, and Edwin K. Silverman
Proceedings of the American Thoracic Society 2008 5: 486-493. [Abstract] [Full Text]  



This article has been cited by other articles:


Home page
 RadioGraphicsHome page
L. Ketai, A. K. Attili, E. A. Kazerooni, B. H. Gross, K. R. Flaherty, J. L. Myers, and F. J. Martinez
Invited Commentary * Authors' Response
RadioGraphics, September 1, 2008; 28(5): 1396 - 1398.
[Full Text] [PDF]


HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Copyright © 2008 by the American Thoracic Society. 		 
Tobacco