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Proteases in COPD : A Critical Pathway to Injury

Gerard M. Turino, MD
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Affiliations: New York, NY ,  Dr. Turino is the John H. Keating Sr Professor of Medicine (Emeritus), Columbia University College of Physicians and Surgeons, and Director, James P. Mara Center for Lung Disease, St. Luke’s-Roosevelt Hospital.

Correspondence to: Gerard M. Turino, MD, St. Luke’s-Roosevelt Hospital Center, 1000 Tenth Ave, New York, NY 10019; e-mail: gmt1@columbia.edu



Chest. 2007;132(6):1724-1725. doi:10.1378/chest.07-1572
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With the discovery of α1-antitrypsin deficiency as a genetically determined predisposition to the development of pulmonary emphysema,1 the concept of enzymatic mechanisms producing lung destruction became a primary avenue of investigation in COPD.2 Earlier studies3 focused on the significance of neutrophil elastase because that is the enzyme for which α1-antitrypsin is a specific inhibitor. More recently, there has been increased awareness of metalloproteases as additional, and possibly more significant pathogenic factors in the development and progression of pulmonary injury in patients with COPD.4

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