全氟和多氟烷基物质 (PFAS) 与妊娠高血压疾病--流行病学和机理证据的整合。

IF 3.3 4区 医学 Q2 REPRODUCTIVE BIOLOGY
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引用次数: 0

摘要

背景:尽管医疗技术在不断进步,但妊娠高血压疾病(HDP)仍然是全球健康的重大负担。妊娠高血压的发病率似乎正在上升,导致孕产妇和胎儿并发症、死亡率和大量医疗费用的增加。HDP 的病因复杂多样,受营养、肥胖、压力、代谢紊乱和遗传等因素的影响。新的证据表明,环境污染物,尤其是全氟和多氟烷基物质(PFAS),可能会导致 HDP 的发生:本综述综合了流行病学和机理数据,探讨了 PFAS 暴露与 HDP 之间错综复杂的关系:研究表明,PFAS 暴露与 HDP 之间存在不同程度的关联,其中一些研究表明两者呈正相关,尤其是与子痫前期。Meta 分析表明,这些关联可能存在胎儿性别差异:从机理上讲,接触 PFAS 似乎会破坏血管血流动力学、胎盘发育以及血管生成和性类固醇调节等关键过程。实验研究显示,肾素-血管紧张素系统、滋养细胞侵袭、氧化应激、炎症和荷尔蒙失调都发生了改变,这些都是导致 HDP 发病的原因。阐明这些机制对于制定预防策略至关重要:治疗潜力:AT2R 激动剂、caspase 抑制剂和特定 microRNAs 调节等靶向干预措施有望减轻孕期接触 PFAS 所导致的不良后果:要全面了解全氟辛烷磺酸诱发的胎盘改变及其对母体和胎儿健康的长期影响,还需要进一步的研究。这些知识将有助于在不断变化的环境中为 HDP 制定有效的预防和治疗策略。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Per- and polyfluoroalkyl substances (PFAS) and hypertensive disorders of Pregnancy- integration of epidemiological and mechanistic evidence

Background

Hypertensive disorders of pregnancy (HDP) remain a significant global health burden despite medical advancements. HDP prevalence appears to be rising, leading to increased maternal and fetal complications, mortality, and substantial healthcare costs. The etiology of HDP are complex and multifaceted, influenced by factors like nutrition, obesity, stress, metabolic disorders, and genetics. Emerging evidence suggests environmental pollutants, particularly Per- and polyfluoroalkyl substances (PFAS), may contribute to HDP development.

Objective

This review integrates epidemiological and mechanistic data to explore the intricate relationship between PFAS exposure and HDP.

Epidemiological evidence

Studies show varying degrees of association between PFAS exposure and HDP, with some demonstrating positive correlations, particularly with preeclampsia. Meta-analyses suggest potential fetal sex-specific differences in these associations.

Mechanistic insights

Mechanistically, PFAS exposure appears to disrupt vascular hemodynamics, placental development, and critical processes like angiogenesis and sex steroid regulation. Experimental studies reveal alterations in the renin-angiotensin system, trophoblast invasion, oxidative stress, inflammation, and hormonal dysregulation – all of which contribute to HDP pathogenesis. Elucidating these mechanisms is crucial for developing preventive strategies.

Therapeutic potential

Targeted interventions such as AT2R agonists, caspase inhibitors, and modulation of specific microRNAs show promise in mitigating adverse outcomes associated with PFAS exposure during pregnancy.

Knowledge gaps and future directions

Further research is needed to comprehensively understand the full spectrum of PFAS-induced placental alterations and their long-term implications for maternal and fetal health. This knowledge will be instrumental in developing effective preventive and therapeutic strategies for HDP in a changing environmental landscape.

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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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