Mechanism of the development of pulmonary emphysema

Tomoko Betsuyaku

Research output: Contribution to journalArticle

Abstract

It is generally accepted that pulmonary emphysema is a consequence of proteinase-antiproteinase imbalance in the lungs, which can be induced by cigarette smoking. Recognition that elastic fiber destruction is probably a central feature in the pathogenesis of smoking-induced emphysema has focused attention on elastolytic enzymes that might be involved. The lungs contain a number of elastolytic enzymes that mainly originate from inflammatory cells such as neutrophils or macrophages that have emigrated into the lungs. Accordingly, it has long been debated which cell and/or which proteinase is mainly responsible for the mechanism of parenchymal destruction associated with cigarette smoking. Structural cells in the lungs such as epithelial cells and endothelial cells may also be involved in cell death and repair. Individual genetic background may regulate the function of these cells in response to cigarette smoke and is related to the susceptibility to pulmonary emphysema.

Original languageEnglish
Pages (from-to)235-245
Number of pages11
JournalConnective Tissue
Volume34
Issue number3
Publication statusPublished - 2002 Sep
Externally publishedYes

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Pulmonary Emphysema
Lung
Smoking
Peptide Hydrolases
Elastic Tissue
Emphysema
Enzymes
Smoke
Tobacco Products
Neutrophils
Cell Death
Endothelial Cells
Epithelial Cells
Macrophages

Keywords

  • Antioxidant, smoking, elastin
  • Antiprotease, oxidant
  • Pulmonary emphysema, protease

ASJC Scopus subject areas

  • Rheumatology

Cite this

Mechanism of the development of pulmonary emphysema. / Betsuyaku, Tomoko.

In: Connective Tissue, Vol. 34, No. 3, 09.2002, p. 235-245.

Research output: Contribution to journalArticle

Betsuyaku, T 2002, 'Mechanism of the development of pulmonary emphysema', Connective Tissue, vol. 34, no. 3, pp. 235-245.
Betsuyaku, Tomoko. / Mechanism of the development of pulmonary emphysema. In: Connective Tissue. 2002 ; Vol. 34, No. 3. pp. 235-245.
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