Center for Perinatal Biology, Loma Linda University School of Medicine, 11234 Anderson Street, Loma Linda, 92350 CA, USA.
Curr Vasc Pharmacol. 2013 Sep;11(5):616-40. doi: 10.2174/1570161111311050006.
This review provides evidence that antenatal hypoxia, which represents a significant and worldwide problem, causes prenatal programming of the lung. A general overview of lung development is provided along with some background regarding transcriptional and signaling systems of the lung. The review illustrates that antenatal hypoxic stress can induce a continuum of responses depending on the species examined. Fetuses and newborns of certain species and specific human populations are well acclimated to antenatal hypoxia. However, antenatal hypoxia causes pulmonary vascular disease in fetuses and newborns of most mammalian species and humans. Disease can range from mild pulmonary hypertension, to severe vascular remodeling and dangerous elevations in pressure. The timing, length, and magnitude of the intrauterine hypoxic stress are important to disease development, however there is also a genetic-environmental relationship that is not yet completely understood. Determining the origins of pulmonary vascular remodeling and pulmonary hypertension and their associated effects is a challenging task, but is necessary in order to develop targeted therapies for pulmonary hypertension in the newborn due to antenatal hypoxia that can both treat the symptoms and curtail or reverse disease progression.
这篇综述提供了证据表明，产前缺氧是一个重大且普遍存在的问题，它会导致肺部的产前编程。本文概述了肺的发育，并介绍了一些关于肺转录和信号系统的背景知识。综述表明，产前低氧应激可以根据所检查的物种诱导一系列的反应。某些物种的胎儿和新生儿以及特定的人类群体对产前缺氧有很好的适应能力。然而，产前缺氧会导致大多数哺乳动物物种和人类的胎儿和新生儿发生肺血管疾病。疾病的范围从轻度肺动脉高压到严重的血管重塑和危险的压力升高。宫内低氧应激的时间、长度和程度对疾病的发展很重要，但也存在遗传-环境的关系，目前还不完全清楚。确定肺血管重塑和肺动脉高压的起源及其相关影响是一项具有挑战性的任务，但为了开发针对因产前缺氧导致的新生儿肺动脉高压的靶向治疗方法，这是必要的，这种方法既能治疗症状，又能遏制或逆转疾病进展。
