The roles of free iron, heme, haemoglobin, and the scavenger proteins haemopexin and alpha‐1‐microglobulin in preeclampsia and fetal growth restriction

氧化应激 子痫前期 内分泌学 内科学 合胞滋养细胞 胎盘 血红素 医学 滋养层 结合珠蛋白 胎儿 怀孕 生物化学 生物 遗传学
作者
Lena Erlandsson,Zahra Masoumi,Lucas R. Hansson,Stefan R. Hansson
出处
期刊:Journal of Internal Medicine [Wiley]
卷期号:290 (5): 952-968 被引量:30
标识
DOI:10.1111/joim.13349
摘要

Preeclampsia (PE) is a complex pregnancy syndrome characterised by maternal hypertension and organ damage after 20 weeks of gestation and is associated with an increased risk of cardiovascular disease later in life. Extracellular haemoglobin (Hb) and its metabolites heme and iron are highly toxic molecules and several defence mechanisms have evolved to protect the tissue.We will discuss the roles of free iron, heme, Hb, and the scavenger proteins haemopexin and alpha-1-microglobulin in pregnancies complicated by PE and fetal growth restriction (FGR).In PE, oxidative stress causes syncytiotrophoblast (STB) stress and increased shedding of placental STB-derived extracellular vesicles (STBEV). The level in maternal circulation correlates with the severity of hypertension and supports the involvement of STBEVs in causing maternal symptoms in PE. In PE and FGR, iron homeostasis is changed, and iron levels significantly correlate with the severity of the disease. The normal increase in plasma volume taking place during pregnancy is less for PE and FGR and therefore have a different impact on, for example, iron concentration, compared to normal pregnancy. Excess iron promotes ferroptosis is suggested to play a role in trophoblast stress and lipotoxicity. Non-erythroid α-globin regulates vasodilation through the endothelial nitric oxide synthase pathway, and hypoxia-induced α-globin expression in STBs in PE placentas is suggested to contribute to hypertension in PE. Underlying placental pathology in PE with and without FGR might be amplified by iron and heme overload causing oxidative stress and ferroptosis. As the placenta becomes stressed, the release of STBEVs increases and affects the maternal vasculature.

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