Baker Christopher D, Alvira Cristina M
aSection of Pulmonary Medicine and Pediatric Heart Lung Center, Department of Pediatrics, University of Colorado School of Medicine, Aurora, Colorado, USA bDepartment of Pediatrics, Center for Excellence in Pulmonary Biology, Stanford University School of Medicine, Stanford, California, USA.
Curr Opin Pediatr. 2014 Jun;26(3):306-14. doi: 10.1097/MOP.0000000000000095.
Advances in medical therapy have increased survival of extremely premature infants and changed the pathology of bronchopulmonary dysplasia (BPD) from one of acute lung injury to a disease of disrupted lung development. With this evolution, new questions emerge regarding the molecular mechanisms that control postnatal lung development, the effect of early disruptions of postnatal lung development on long-term lung function, and the existence of endogenous mechanisms that permit lung regeneration after injury.
Recent data demonstrate that a significant component of alveolarization, the final stage of lung development, occurs postnatally. Further, clinical and experimental studies demonstrate that premature birth disrupts alveolarization, decreasing the gas exchange surface area of the lung and causing BPD. BPD is associated with significant short-term morbidity, and new longitudinal, clinical data demonstrate that survivors of BPD have long-standing deficits in lung function and may be at risk for the development of additional lung disease as adults. Unfortunately, current care is mainly supportive with few effective therapies that prevent or treat established BPD. These studies underscore the need to further elucidate the mechanisms that direct postnatal lung growth and develop innovative strategies to stimulate lung regeneration.
Despite significant improvements in the care and survival of extremely premature infants, BPD remains a major clinical problem. Although efforts should remain focused on the prevention of preterm labor and BPD, novel research aimed at promoting postnatal alveolarization offers a unique opportunity to develop effective strategies to treat established BPD.
医学治疗的进展提高了极早产儿的存活率，并使支气管肺发育不良（BPD）的病理从急性肺损伤转变为肺发育受阻的疾病。随着这种演变，出现了关于控制出生后肺发育的分子机制、出生后肺发育早期中断对长期肺功能的影响以及损伤后允许肺再生的内源性机制的存在等新问题。
最近的数据表明，肺发育的最后阶段——肺泡化的一个重要部分发生在出生后。此外，临床和实验研究表明，早产会破坏肺泡化，减少肺的气体交换表面积并导致BPD。BPD与严重的短期发病率相关，新的纵向临床数据表明，BPD幸存者的肺功能长期存在缺陷，成年后可能有患其他肺部疾病的风险。不幸的是，目前的治疗主要是支持性的，很少有有效的疗法来预防或治疗已确诊的BPD。这些研究强调需要进一步阐明指导出生后肺生长的机制，并开发创新策略来刺激肺再生。
尽管极早产儿的护理和存活率有了显著提高，但BPD仍然是一个主要的临床问题。虽然应继续致力于预防早产和BPD，但旨在促进出生后肺泡化的新研究为开发治疗已确诊BPD的有效策略提供了独特的机会。
