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Role of angiogenic factors in the pathogenesis and management of pre‐eclampsia

机译:血管生成因子在预痫前的发病机制和管理中的作用

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摘要

Abstract The cause of pre‐eclampsia is unknown. Different postulates have been developed to explain its pathogenesis. The two‐stage theory and angiogenic imbalance are two notable postulates of the disease. Together, they propose that there is a lack of cytotrophoblastic invasion of the uterine spiral arteries in pre‐eclampsia. The lumen of these arteries remains narrow instead of converting to the wide channels seen in normal pregnancy, and result in poor placental perfusion. Coupled with maternal susceptibility, this process leads to the release of mediators, including an excess of anti‐angiogenic factors that result in the clinical manifestations of the disease. Circulating levels of anti‐angiogenic factors such as soluble fms‐like tyrosine kinase‐1 increase, whereas pro‐angiogenic factors such as placental growth factor decrease. Assessment of the circulating concentrations of these angiogenic factors, such as the soluble fms‐like tyrosine kinase‐1/placental growth factor ratio, has diverse clinical relevance in pre‐eclampsia. The present review describes the role of angiogenic factors in the pathogenesis and management of pre‐eclampsia.
机译:摘要预先普利榜预先的原因未知。已经开发出不同的假设来解释其发病机制。两阶段理论和血管生成不平衡是疾病的两个显着假设。他们建议缺乏异蚊螺旋动脉患有子宫螺旋动脉的细胞萎缩侵袭。这些动脉的内腔仍然狭窄,而不是转换为正常妊娠中看到的宽渠道,导致胎盘灌注不良。再加上母体易感性,该过程导致介质的释放,包括过量的抗血管生成因子,导致疾病的临床表现。循环水平的抗血管生成因子,如可溶性FMS样酪氨酸激酶-1的增加,而诸如胎盘生长因子的促血管生成因子降低。评估这些血管生成因子的循环浓度,例如可溶性的FMS样酪氨酸激酶-1 /胎盘生长因子比,在预先印痫症中具有多种临床相关性。本综述描述了血管生成因子在预先发病机制和管理中的作用。

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