Preeclampsia and transport of ions and small molecules: A literature review

IF 3 2区 医学 Q2 DEVELOPMENTAL BIOLOGY Placenta Pub Date : 2024-09-14 DOI:10.1016/j.placenta.2024.09.009
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Abstract

Preeclampsia (PE) is a prevalent obstetric complication affecting approximately 3–5% of pregnancies worldwide and is a major cause of maternal and perinatal morbidity and mortality. Preeclampsia is considered a disease of the endothelial system that can progress to eclampsia, characterized by seizures. Early diagnosis and appropriate management are crucial to improving maternal and fetal outcomes, as preeclampsia can lead to severe complications such as placental abruption, fetal growth restriction, and stroke. The pathophysiology of PE is complex, involving a combination of genetic, acquired, and immunological factors. A central feature of the condition is inadequate placentation and impaired uteroplacental perfusion, leading to local hypoxia, endothelial dysfunction, vasoconstriction, and immunological dysregulation. Recent evidence suggests that dysregulation of ion transporters may play a significant role in the adaptation of uterine circulation during placentation. These transporters are essential for maintaining maternal-fetal homeostasis, influencing processes such as nutrient exchange, hormone synthesis, trophoblast cell migration, and the function of smooth muscle cells in blood vessels. In preeclampsia, adverse conditions like hypoxia and oxidative stress result in the downregulation of ion, solute, and water transporters, impairing their function. This review focuses on membrane transporters involved in PE, discussing functional alterations and their physiological implications. The goal of this investigation is to enhance understanding of how dysregulation of ion and small molecule transporters contributes to the development and progression of preeclampsia, underscoring the importance of exploring these signaling pathways for potential therapeutic interventions.

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子痫前期与离子和小分子的运输:文献综述
子痫前期(PE)是一种常见的产科并发症,影响着全球约 3%-5% 的妊娠,是孕产妇和围产期发病率和死亡率的主要原因。子痫前期被认为是一种内皮系统疾病,可发展为子痫,其特点是癫痫发作。由于子痫前期可导致胎盘早剥、胎儿生长受限和中风等严重并发症,因此早期诊断和适当治疗对改善母体和胎儿的预后至关重要。子痫前期的病理生理学非常复杂,涉及遗传、获得性和免疫因素的综合作用。其核心特征是胎盘功能不足和子宫胎盘灌注受损,导致局部缺氧、内皮功能障碍、血管收缩和免疫调节失调。最近的证据表明,离子转运体的失调可能在胎盘期子宫循环的适应中起着重要作用。这些转运体对维持母胎平衡至关重要,影响着营养交换、激素合成、滋养层细胞迁移和血管平滑肌细胞功能等过程。在子痫前期,缺氧和氧化应激等不利条件会导致离子、溶质和水转运体下调,从而损害其功能。本综述将重点关注参与子痫前期的膜转运体,讨论其功能改变及其生理影响。这项研究的目的是加深对离子和小分子转运体失调如何导致子痫前期发生和发展的认识,强调探索这些信号通路对潜在治疗干预的重要性。
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来源期刊
Placenta
Placenta 医学-发育生物学
CiteScore
6.30
自引率
10.50%
发文量
391
审稿时长
78 days
期刊介绍: Placenta publishes high-quality original articles and invited topical reviews on all aspects of human and animal placentation, and the interactions between the mother, the placenta and fetal development. Topics covered include evolution, development, genetics and epigenetics, stem cells, metabolism, transport, immunology, pathology, pharmacology, cell and molecular biology, and developmental programming. The Editors welcome studies on implantation and the endometrium, comparative placentation, the uterine and umbilical circulations, the relationship between fetal and placental development, clinical aspects of altered placental development or function, the placental membranes, the influence of paternal factors on placental development or function, and the assessment of biomarkers of placental disorders.
期刊最新文献
Corrigendum to “Unveiling placental development in circadian rhythm-disrupted mice: A photo-acoustic imaging study on unstained tissue” [Placenta 158 (2024) 57-61] Placental extracellular vesicles promoted cervical tumour tissue undergoing death Feto-placental vascular structure and in silico haemodynamics: Of mice, rats, and human Endothelin-1 potentiated constriction in preeclampsia placental veins: Role of ETAR/ETBR/CaV1.2/CALD1 Placenta-associated biomarkers and pregnancy outcome in HPA-1a alloimmunization: A prospective cohort study
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