Epigenetic contributions to the developmental origins of adult lung disease

被引:21
作者
Joss-Moore, Lisa A. [1 ]
Lane, Robert H. [2 ]
Albertine, Kurt H. [1 ]
机构
[1] Univ Utah, Div Neonatol, Dept Pediat, Salt Lake City, UT 84158 USA
[2] Med Coll Wisconsin, Dept Pediat, Milwaukee, WI 53226 USA
关键词
lung development; epigenetic; developmental origins; programming; ACTIVATED RECEPTOR-GAMMA; GROWTH-FACTOR-BETA; NEONATAL-RAT LUNG; DNA METHYLATION; MATERNAL SMOKING; PPAR-GAMMA; HISTONE ACETYLATION; BRONCHOPULMONARY DYSPLASIA; RESPIRATORY HEALTH; ALVEOLAR FORMATION;
D O I
10.1139/bcb-2014-0093
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
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.
引用
收藏
页码:119 / 127
页数:9
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