Bronchopulmonary dysplasia (BPD) is a multifactorial disease occurring as a consequence of premature birth, as well as antenatal and postnatal injury to the developing lung. BPD morbidity and severity depend on a complex interplay between prenatal and postnatal inflammation, mechanical ventilation, and oxygen therapy as well as associated prematurity-related complications. These initial hits result in ill-explored aberrant immune and reparative response, activation of pro-fibrotic and anti-angiogenic factors, which further perpetuate the injury. Histologically, the disease presents primarily by impaired lung development and an arrest in lung microvascular maturation. Consequently, BPD leads to respiratory complications beyond the neonatal period and may result in premature aging of the lung. While the numerous prenatal and postnatal stimuli contributing to BPD pathogenesis are relatively well known, the specific cell populations driving the injury, as well as underlying mechanisms are still not well understood. Recently, an effort to gain a more detailed insight into the cellular composition of the developing lung and its progenitor populations has unfold. Here, we provide an overview of the current knowledge regarding perinatal origin of BPD and discuss underlying mechanisms, as well as novel approaches to study the perturbed lung development.

中文翻译：

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支气管肺发育不良的围产期起源——逐个细胞解读正常和受损的肺发育

支气管肺发育不良 (BPD) 是一种多因素疾病，由早产以及发育中的肺部的产前和产后损伤引起。BPD 的发病率和严重程度取决于产前和产后炎症、机械通气和氧疗以及相关早产相关并发症之间复杂的相互作用。这些最初的打击导致了未经探索的异常免疫和修复反应，激活了促纤维化和抗血管生成因子，从而进一步使损伤永久化。在组织学上，该疾病主要表现为肺发育受损和肺微血管成熟停滞。因此，BPD 会导致新生儿期以外的呼吸系统并发症，并可能导致肺部过早老化。虽然导致 BPD 发病机制的众多产前和产后刺激相对众所周知，但驱动损伤的特定细胞群以及潜在机制仍不清楚。最近，人们开始努力更详细地了解发育中的肺及其祖细胞群的细胞组成。在这里，我们概述了有关 BPD 围产期起源的当前知识，并讨论了潜在的机制以及研究肺部发育紊乱的新方法。