Joss-Moore Lisa A, Lane Robert H, Albertine Kurt H
Division of Neonatology, Department of Pediatrics, University of Utah, P.O. Box 581289, Salt Lake City, UT 84158, USA.
Biochem Cell Biol. 2015 Apr;93(2):119-27. doi: 10.1139/bcb-2014-0093. Epub 2014 Oct 13.
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.
围产期损伤,包括子宫内生长受限、早产、母亲接触毒素或饮食缺乏,会导致肺细胞表观基因组出现偏差。围产期损伤的发生通常与肺发育的最后阶段同时出现。在肺发育过程中,对围产期损伤作出反应的表观基因组破坏的结果可能是肺的长期结构和功能损害以及肺部疾病的发展。了解表观遗传机制对围产期损伤后终身肺部疾病的作用是成人肺部疾病发育起源领域的研究重点。在各种形式的肺部疾病中均观察到DNA甲基化、组蛋白修饰和微小RNA变化。然而,围产期对这些表观遗传机制的作用却知之甚少。在此,我们讨论成人肺部疾病的发育起源、围产期事件、肺发育与疾病之间的相互作用,以及表观遗传机制在连接这些事件中所起的作用。