内分泌干扰物在子痫前期的潜在作用:基于流行病学和实验证据的综合假设。

IF 2.8 4区 医学 Q2 REPRODUCTIVE BIOLOGY
Bárbara Campos Jorge , Julia Polotto da Silva , Sara Tawany Caetano dos Santos , Fernando Barbosa , Valéria Cristina Sandrim , Arielle Cristina Arena
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引用次数: 0

摘要

子痫前期(PE)是一种复杂的高血压疾病,是全世界孕产妇和围产期发病率的主要原因。新出现的证据表明,暴露于内分泌干扰化学物质(EDCs)可能与PE的病因有关,但这种关联仍未得到充分探讨。本综述旨在调查流行病学和实验研究,评估EDC暴露与PE发展之间的潜在联系。通过PubMed、ScienceDirect和b谷歌Scholar对过去十年发表的原创文章进行了文献检索。选择了40项研究,包括流行病学队列,体内和体外模型,重点关注EDCs与PE或相关生物标志物之间的关联。流行病学调查结果是异质的:虽然大型队列通常没有显示关联,但一些病例对照研究将特定的EDCs(如双酚A、邻苯二甲酸盐、镉和全氟辛烷磺酸)与PE风险增加和血压升高联系起来。实验证据显示,EDCs损害关键的胎盘过程,包括去个体化、血管生成和滋养细胞侵袭。这些破坏通常伴随着氧化应激、激素失衡和内皮功能障碍,这是PE发病机制的中心特征。体内模型在EDC暴露后也复制了pe样综合征。尽管目前的流行病学证据仍不一致,但机制研究强烈支持EDC参与PE的生物学合理性。这篇综述强调,EDCs对PE的贡献可能被低估,并呼吁进行多学科研究,以澄清暴露阈值、脆弱窗口和人群特异性易感性。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Potential role of endocrine-disrupting chemicals in preeclampsia: A hypothesis based on integration of epidemiological and experimental evidence
Preeclampsia (PE) is a complex hypertensive disorder and a leading cause of maternal and perinatal morbidity worldwide. Emerging evidence suggests that exposure to endocrine-disrupting chemicals (EDCs) may contribute to the etiology of PE, yet this association remains underexplored. This review aimed to investigate epidemiological and experimental studies assessing the potential link between EDC exposure and PE development. A literature search was conducted across PubMed, ScienceDirect, and Google Scholar for original articles published in the last ten years. Forty studies were selected, including epidemiological cohorts, in vivo, and in vitro models, focusing on the association between EDCs and PE or related biomarkers. Epidemiological findings were heterogeneous: while large cohorts often showed no association, several case-control studies linked specific EDCs, such as bisphenol A, phthalates, cadmium, and PFOS, to increased PE risk and elevated blood pressure. Experimental evidence revealed that EDCs impair key placental processes, including decidualization, angiogenesis, and trophoblast invasion. These disruptions were often accompanied by oxidative stress, hormonal imbalances, and endothelial dysfunction, central features in PE pathogenesis. In vivo models also replicated PE-like syndrome after EDC exposure. Although current epidemiological evidence remains inconsistent, mechanistic studies strongly support the biological plausibility of EDC involvement in PE. This review highlights that the contribution of EDCs to PE may be underestimated and calls for multidisciplinary research to clarify exposure thresholds, vulnerable windows, and population-specific susceptibilities.
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来源期刊
Reproductive toxicology
Reproductive toxicology 生物-毒理学
CiteScore
6.50
自引率
3.00%
发文量
131
审稿时长
45 days
期刊介绍: Drawing from a large number of disciplines, Reproductive Toxicology publishes timely, original research on the influence of chemical and physical agents on reproduction. Written by and for obstetricians, pediatricians, embryologists, teratologists, geneticists, toxicologists, andrologists, and others interested in detecting potential reproductive hazards, the journal is a forum for communication among researchers and practitioners. Articles focus on the application of in vitro, animal and clinical research to the practice of clinical medicine. All aspects of reproduction are within the scope of Reproductive Toxicology, including the formation and maturation of male and female gametes, sexual function, the events surrounding the fusion of gametes and the development of the fertilized ovum, nourishment and transport of the conceptus within the genital tract, implantation, embryogenesis, intrauterine growth, placentation and placental function, parturition, lactation and neonatal survival. Adverse reproductive effects in males will be considered as significant as adverse effects occurring in females. To provide a balanced presentation of approaches, equal emphasis will be given to clinical and animal or in vitro work. Typical end points that will be studied by contributors include infertility, sexual dysfunction, spontaneous abortion, malformations, abnormal histogenesis, stillbirth, intrauterine growth retardation, prematurity, behavioral abnormalities, and perinatal mortality.
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