Perinatal origins of bronchopulmonary dysplasia-deciphering normal and impaired lung development cell by cell.

IF 2.4 Q1 PEDIATRICS
I Mižíková, B Thébaud
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引用次数: 2

Abstract

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.

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,由于早产以及产前和产后对发育中的肺的损伤而发生。BPD的发病率和严重程度取决于产前和产后炎症、机械通气、氧疗以及相关的早产相关并发症之间的复杂相互作用。这些最初的撞击导致未被充分探索的异常免疫和修复反应,促纤维化和抗血管生成因子的激活,进一步使损伤永久化。组织学上,该病主要表现为肺发育受损和肺微血管成熟停止。因此,BPD会导致新生儿期以后的呼吸系统并发症,并可能导致肺部过早衰老。虽然许多产前和产后刺激对BPD发病机制的影响相对已知,但驱动损伤的特定细胞群及其潜在机制仍未得到很好的理解。最近,一项努力,以获得更详细的洞察细胞组成的发展中的肺和它的祖先群体已经展开。在这里,我们概述了目前关于BPD围产期起源的知识,并讨论了潜在的机制,以及研究肺发育紊乱的新方法。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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CiteScore
2.20
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0.00%
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