Hubel C A
Magee-Womens Research Institute, Pittsburgh, PA 15213, USA.
Semin Reprod Endocrinol. 1998;16(1):75-92. doi: 10.1055/s-2007-1016255.
The etiology and pathogenesis of the pregnancy syndrome preeclampsia remain poorly understood. There is evidence that oxidative stress (am imbalance between oxidant and antioxidant forces in favor of oxidants) occurs in preeclampsia, and it has been hypothesized that reactive oxygen species or their metabolites ultimately comprise the "defensive" vasodilatory, antiaggregatory, and barrier functioning of the vascular endothelium. Oxidative stress may be point at which feto-placental and maternal factors converge, resulting in the protean manifestations of preeclampsia. This review highlights the evidence for maternal dyslipidemia and altered iron kinetics in preeclampsia and gives a critical assessment of their potential impact on disease progression. The theme is developed that interaction of maternal components, particularly neutrophils and oxidation-susceptible lipids, with placental cells and placental-derived factors engenders feed-forward cycles of oxidative stress that ultimately cause widespread endothelial cell dysfunction and its clinical manifestations.
妊娠综合征子痫前期的病因和发病机制仍未得到充分了解。有证据表明,子痫前期会出现氧化应激(氧化剂和抗氧化剂力量失衡,氧化剂占优势),并且有人推测活性氧或其代谢产物最终会破坏血管内皮的“防御性”血管舒张、抗聚集和屏障功能。氧化应激可能是胎儿 - 胎盘因素和母体因素交汇的关键点,从而导致子痫前期的多种表现。本综述强调了子痫前期母体血脂异常和铁动力学改变的证据,并对它们对疾病进展的潜在影响进行了批判性评估。本文提出的观点是,母体成分,特别是中性粒细胞和易氧化脂质,与胎盘细胞和胎盘衍生因子的相互作用会引发氧化应激的前馈循环,最终导致广泛的内皮细胞功能障碍及其临床表现。