title: The importance of epigenetics in the development of chronic obstructive pulmonary disease.
abstract: It is generally accepted that genetic predisposition plays a role in COPD development in susceptible individuals. Therefore, many candidate genes that could be linked to the development of disease have been examined in COPD. However, inconsistent results in different study populations often limit this approach, suggesting that not only genetics, but also other factors, may be contributed to the susceptibility to COPD. Epigenetic mechanisms can affect the transcriptional activity of specific genes, at different points in time, and in different organs. Moreover, these mechanisms can have an effect on people's health. Recently, there is emerging evidence supporting a role of epigenetics for the regulation of inflammatory genes in diseases such as asthma and COPD. Moreover, recent studies suggest that the currently used treatments including corticosteroids may work through epigenetic mechanisms. Epigenetic regulation can be reprogrammed, potentially affecting the risk, aetiology and treatment of various disease states. The epigenetically influenced phenotype could be reversed with demethylating or deacetylating agents, consistent with epigenetic plasticity. The postnatal reversibility of these methylation or acetylation events may therefore provide good opportunities for intervention. The recognition of the role of genetic and epigenetic mechanisms in the development of COPD may identify novel targets that hatch new therapies for patients with COPD.
authors.affiliation: Department of Respirology (B2), Graduate School of Medicine, Chiba University, Chuo-ku, Chiba, Japan. sakaos@faculty.chiba-u.jp
authors.forename: Seiichiro
authors.initials: S
authors.lastname: Sakao
authors.forename: Koichiro
authors.initials: K
authors.lastname: Tatsumi
mesh_terms: D018450:Disease Progression; D044127:Epigenesis, Genetic; D020022:Genetic Predisposition to Disease; D006801:Humans; D007249:Inflammation / Q000235:genetics; D010641:Phenotype; D029424:Pulmonary Disease, Chronic Obstructive / Q000453:epidemiology / Q000209:etiology / Q000235:genetics*; D015533:Transcriptional Activation / Q000235:genetics*