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Abstract
Preeclampsia is one of the most common complications of pregnancy that is prevalent worldwide, resulting in substantial maternal and neonatal morbidity and mortality. Although the cause remains unclear, preeclampsia may be initiated by abnormal placentation and reduced placental perfusion, followed by an imbalance of angiogenic and antiangiogenic factors and subsequent systemic endothelial dysfunction. High level of antiangiogenic factors, such as soluble vascular endothelial growth factor (VEGF) receptor 1 (sVEGFR-1, also known as sFlt-1) and soluble endoglin, and low levels of angiogenic factors, such as free maternal VEGF and placental growth factor (PlGF), are associated with preeclampsia. Angiogenic and antiangiogenic factors also play an important role during lung angiogenesis, and an imbalance between the two types of factors triggered by inflammation disrupts angiogenesis in bronchopulmonary dysplasia (BPD). Because preeclampsia represents an antiangiogenic state, preterm infants born to mothers with preeclampsia would be at increased risk of developing BPD due to impaired lung development. Recently, preeclampsia has been shown to be independently associated with a high risk for BPD. I have reviewed recent progress in research concerning the correlation between preeclampsia and BPD in aspect of pathophysiology and epidemiology.
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Fig. 2.
Abnormal placentation in preeclampsia. In normal placental development, invasive cytotrophoblasts of fetal origin invade the maternal spiral arteries, transforming them from small-caliber resistance vessels to high-caliber capacitance vessels capable of providing placental perfusion adequate to sustain the growing fetus. In preeclampsia, invasion of the spiral arteries is shallow, and they remain small-caliber, resistance vessels (lower panel). Adopted from Hypertension 2005;46:1077–85.14
Fig. 3.
(A) Effects of intra-amniotic sFlt-1 treatment on distal lung growth in 14-day-old rats; lung histology was stained with hematoxylin and eosin. sFlt-1 rats demonstrated simplified alveoli (A-1), decreased radial alveolar counts, increased mean linear intercept, and reduced nodal point density (A-2), compared with the control. (B) Effects of intra-amniotic sFlt-1 treatment on pulmonary vessel density in lung histology stained with von Willebrand Factor (vWF) from 14-day-old rats. Pulmonary vessel density was reduced in sFlt-1 rats as shown by histology (B-1) and documented by morphometric analysis (B-2). Adopted from Am J Physiol Lung Cell Mol Physiol 2012;302:L36–46.9
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