Epigenetic contributions to the developmental origins of adult lung disease. Biochem Cell Biol 2015 Apr;93(2):119-27
Date
12/11/2014Pubmed ID
25493710Pubmed Central ID
PMC5683896DOI
10.1139/bcb-2014-0093Scopus ID
2-s2.0-84964304821 (requires institutional sign-in at Scopus site) 31 CitationsAbstract
Perinatal insults, including intrauterine growth restriction, preterm birth, maternal exposure to toxins, or dietary deficiencies produce deviations in the epigenome of lung cells. Occurrence of perinatal insults often coincides with the final stages of lung development. The result of epigenome disruptions in response to perinatal insults during lung development may be long-term structural and functional impairment of the lung and development of lung disease. Understanding the contribution of epigenetic mechanisms to life-long lung disease following perinatal insults is the focus of the developmental origins of adult lung disease field. DNA methylation, histone modifications, and microRNA changes are all observed in various forms of lung disease. However, the perinatal contribution to such epigenetic mechanisms is poorly understood. Here we discuss the developmental origins of adult lung disease, the interplay between perinatal events, lung development and disease, and the role that epigenetic mechanisms play in connecting these events.
Author List
Joss-Moore LA, Lane RH, Albertine KHMESH terms used to index this publication - Major topics in bold
AdultAnimals
DNA Methylation
Disease Models, Animal
Epigenesis, Genetic
Female
Gene Expression Regulation, Developmental
Histones
Humans
Lung
Lung Diseases
Male
Mice
MicroRNAs
Pregnancy
Rats
Sheep
