Abstract
Chronic obstructive pulmonary disease (COPD) is a smoking-related disorder in which inflammation occurs in the small airways and lung parenchyma, and results in progressive airflow limitation leading to respiratory failure and death. Inflammatory mediators are continuously released due to increased transcription of their corresponding genes. This can be favoured by chromatin remodelling (i.e., by an imbalance between histone acetyltransferases [transcription accelerators] and histone deacetylases [transcription supressors] produced either by increased activity of the former and/or reduced activity of the latter). In the present study, a decreased HDAC activity (particularly of isoform 2) is reported in vitro in specimens from COPD patients, correlating with disease severity and inflammatory gene expression. This finding could explain therapeutic refractoriness and perpetuation of inflammation and could reveal an evolving therapeutic target in COPD.
Published Version
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