Department of Biomedical Engineering, George Washington University, 800 22nd Street NW, Washington, DC 20052, USA.
Department of Anatomy, Biochemistry & Physiology, Johns A. Burns School of Medicine, University of Hawaii, 651 Ilalo Street, Honolulu, HI 96813, USA.
Int J Mol Sci. 2021 Sep 1;22(17):9523. doi: 10.3390/ijms22179523.
Pediatric obstructive sleep apnea has significant negative effects on health and behavior in childhood including depression, failure to thrive, neurocognitive impairment, and behavioral issues. It is strongly associated with an increased risk for chronic adult disease such as obesity and diabetes, accelerated atherosclerosis, and endothelial dysfunction. Accumulating evidence suggests that adult-onset non-communicable diseases may originate from early life through a process by which an insult applied at a critical developmental window causes long-term effects on the structure or function of an organism. In recent years, there has been increased interest in the role of epigenetic mechanisms in the pathogenesis of adult disease susceptibility. Epigenetic mechanisms that influence adaptive variability include histone modifications, non-coding RNAs, and DNA methylation. This review will highlight what is currently known about the phenotypic associations of epigenetic modifications in pediatric obstructive sleep apnea and will emphasize the importance of epigenetic changes as both modulators of chronic disease and potential therapeutic targets.
小儿阻塞性睡眠呼吸暂停对儿童时期的健康和行为有显著的负面影响,包括抑郁、生长发育不良、神经认知障碍和行为问题。它与肥胖和糖尿病、动脉粥样硬化加速和内皮功能障碍等慢性成人疾病的风险增加密切相关。越来越多的证据表明,成人发病的非传染性疾病可能起源于生命早期,这一过程是通过在关键发育窗口施加的一种损伤对生物体的结构或功能产生长期影响来实现的。近年来,人们对表观遗传机制在成人疾病易感性发病机制中的作用产生了越来越大的兴趣。影响适应性变异性的表观遗传机制包括组蛋白修饰、非编码 RNA 和 DNA 甲基化。这篇综述将重点介绍目前已知的小儿阻塞性睡眠呼吸暂停中表观遗传修饰的表型相关性,并强调了表观遗传变化作为慢性疾病的调节剂和潜在治疗靶点的重要性。