Linked Life Data

3298671

Source:http://linkedlifedata.com/resource/pubmed/id/3298671

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2
pubmed:dateCreated
1987-8-4
pubmed:abstractText
Emphysema is believed to result from destruction of elastic fibers due to an imbalance between proteases and their inhibitors in the lung. The imbalance can arise from a primary failure of secretion of the inhibitors, as occurs in hereditary alpha-1-protease inhibitor deficiency, or as the result of complex interactions of environmental agents with the lung. Environmental agents may produce their effects by stimulating degradation of elastic fibers by neutrophils and macrophages, damaging protease inhibitors by oxidative or proteolytic mechanisms or by impairing the biosynthetic repair of damage to the connective tissue. Protease excess has also been consistently observed in purulent sputum. Since experimentally administered proteases stimulate secretion of mucus and damage mucociliary clearance, protease-antiprotease imbalance might be involved in the pathogenesis of bronchitis and bronchiectasis as well as emphysema. Because the protease inhibitors of bronchial mucus are distinct from those of the acinar units, and no hereditary deficiencies are known, there is no direct proof of this hypothesis in man.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Mar
pubmed:issn
0883-5993
pubmed:author
pubmed:issnType
Print
pubmed:volume
1
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
1-6
pubmed:dateRevised
2004-11-17
pubmed:meshHeading
pubmed:year
1986
pubmed:articleTitle
The biochemical pathogenesis of chronic obstructive pulmonary diseases: protease-antiprotease imbalance in emphysema and diseases of the airways.
pubmed:publicationType
Journal Article, Review