PDF(Pubmed)
Abstract：
Clinically, intrauterine hypoxia is the foremost cause of perinatal morbidity and developmental plasticity in the fetus and newborn infant. Under hypoxia, deviations occur in the lung cell epigenome. Epigenetic mechanisms (e.g., DNA methylation, histone modification, and miRNA expression) control phenotypic programming and are associated with physiological responses and the risk of developmental disorders, such as bronchopulmonary dysplasia. This developmental disorder is the most frequent chronic pulmonary complication in preterm labor. The pathogenesis of this disease involves many factors, including aberrant oxygen conditions and mechanical ventilation-mediated lung injury, infection/inflammation, and epigenetic/genetic risk factors. This review is focused on various aspects related to intrauterine hypoxia and epigenetic programming in lung development and disease, summarizes our current knowledge of hypoxia-induced epigenetic programming and discusses potential therapeutic interventions for lung disease.
摘要：
临床上,宫内缺氧是胎儿和新生儿围产期发病和发育可塑性的首要原因。在缺氧下，肺细胞表观基因组出现偏差。表观遗传机制(例如，DNA甲基化，组蛋白修饰，和miRNA表达）控制表型编程，并与生理反应和发育障碍的风险相关，如支气管肺发育不良。这种发育障碍是早产中最常见的慢性肺部并发症。本病的发病机制涉及多种因素,包括异常氧气条件和机械通气介导的肺损伤，感染/炎症，和表观遗传/遗传风险因素。本文就宫内缺氧和表观遗传编程在肺发育和疾病相关的各个方面进行综述。总结了我们目前对缺氧诱导的表观遗传编程的认识，并讨论了对肺部疾病的潜在治疗干预措施。
