Abstract
Although much remains to be done, recent advances and the advent of new methodologies are promising and should yield increased understanding of the genetic and epigenetic mechanisms influencing the pathogenesis of COPD, both related and unrelated to severe AAT deficiency. Such understanding should ultimately be translated into novel approaches to prevent, diagnose, and treat COPD.
Copyright © 2012 Elsevier Inc. All rights reserved.
Publication types
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Research Support, N.I.H., Extramural
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Research Support, Non-U.S. Gov't
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Review
MeSH terms
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Epigenesis, Genetic
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Forced Expiratory Volume / genetics
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Genetic Markers
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Genome-Wide Association Study
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Humans
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Phenotype
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Polymorphism, Single Nucleotide
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Pulmonary Disease, Chronic Obstructive / etiology
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Pulmonary Disease, Chronic Obstructive / genetics*
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Risk Factors
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Smoking / adverse effects
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Vital Capacity / genetics
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alpha 1-Antitrypsin / genetics*
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alpha 1-Antitrypsin Deficiency / complications*
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alpha 1-Antitrypsin Deficiency / diagnosis
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alpha 1-Antitrypsin Deficiency / genetics
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alpha 1-Antitrypsin Deficiency / therapy
Substances
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Genetic Markers
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SERPINA1 protein, human
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alpha 1-Antitrypsin