The Biochemical Basis of Emphysema: the Oxidant Effect of Cigarette Smoke?

  1. PHILIP KIMBEL, M.D.; and
  2. FRIEDRICH KUEPPERS, M.D.
  1. Department of Medicine, Graduate Hospital and University of Pennsylvania
  2. Pulmonary Division, Temple University School of Medicine;
    Philadelphia, Pennsylvania

    Excerpt

    Major advances in medicine are marked by the unraveling of the biochemical mechanisms of important diseases. Such an advance now seems near for pulmonary emphysema. Current research was stimulated by the discovery and description of alpha1-antitrypsin deficiency-related emphysema, a genetically determined disease (1), and the development of animal models of emphysema induced by proteases from neutrophil granulocytes (2). These observations have led to the hypothesis that emphysema results from degradation of lung elastin, an important connective tissue component of pulmonary parenchyma. The elastolysis is in turn produced by an imbalance in the lungs between elastase and its inhibitors when elastase

    This 100-word excerpt has been provided in the absence of an abstract.

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