Epigenetics and the developmental origins of lung disease

Abstract: The developmental origins of disease hypothesis have recently been expanded to include the early origins of lung disease, particularly early events that alter lung development. Intrauterine growth restriction (IUGR), preterm birth with the need for prolonged mechanical ventilation, and maternal tobacco smoke (MTS) or nicotine exposure produce neonatal and adult lung disease. These perinatal insults are characterized by alterations in alveolar formation and changes in the expression of genes that regulate alveolarization, including IGF1 and PPARγ. A potential mechanism for such changes in gene expression is epigenetics. IGF1 and PPARγ have altered epigenetic states in response to these perinatal insults. Identification of the specific epigenetic mechanisms involved in the developmental origin of lung disease may facilitate identification of molecular biomarkers with the potential to personalize respiratory disease risk assessment and treatment. The purpose of this review is to summarize what is known about the developmental origins of lung disease, the epigenetic contributions to lung disease, and areas that need further investigation. [Copyright &y& Elsevier]

Copyright of Molecular Genetics & Metabolism is the property of Academic Press Inc. and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)