Molecular signature of cadmium-mediated neurodevelopmental disorders in prenatal to postnatal stages.

IF 4.9 3区 生物学 Q1 BIOLOGY
EXCLI Journal Pub Date : 2025-07-17 eCollection Date: 2025-01-01 DOI:10.17179/excli2025-8322
Sabiha Sultana Preety, Fahim Rejanur Tasin, Amit Sarder, Debasish Halder, Farjana Yasmin, Chanchal Mandal
{"title":"Molecular signature of cadmium-mediated neurodevelopmental disorders in prenatal to postnatal stages.","authors":"Sabiha Sultana Preety, Fahim Rejanur Tasin, Amit Sarder, Debasish Halder, Farjana Yasmin, Chanchal Mandal","doi":"10.17179/excli2025-8322","DOIUrl":null,"url":null,"abstract":"<p><p>Cadmium can surpass fetal circulation and the blood-brain barrier due to its similar physicochemical properties to those of other divalent metals and causes diverse neuronal disorders. Previous reports have suggested a possible link between epigenetic alterations and neuronal changes in offspring due to cadmium exposure at different developmental stages. Hypermethylation of the glucocorticoid receptor NR3C1 disturbs the development of the hypothalamic-pituitary-adrenal axis, which in turn is responsible for the abnormal cognitive behavior of neonates. In addition, the upregulation of placental miR-509-3p and miR-193-5p expression was found to be the major cause of impaired development of the central nervous system. In this review, the epigenetic mechanism of cadmium-mediated neurotoxicity is described. Moreover, the journey of cadmium from the maternal body to the fetal body through circulation and to the neonatal body through breast milk is also tracked. The vulnerability of developing fetuses to cadmium is an alarming issue. Different types of epigenetic changes, such as DNA methylation, altered miRNA expression and histone modifications, are induced by cadmium and lead to various types of neurodevelopmental disorders. We hope this narrative review will provide distinct knowledge of the transportation of cadmium and its adverse effects on fetal neurodevelopment. See also the graphical abstract(Fig. 1).</p>","PeriodicalId":12247,"journal":{"name":"EXCLI Journal","volume":"24 ","pages":"797-823"},"PeriodicalIF":4.9000,"publicationDate":"2025-07-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12419453/pdf/","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"EXCLI Journal","FirstCategoryId":"99","ListUrlMain":"https://doi.org/10.17179/excli2025-8322","RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"2025/1/1 0:00:00","PubModel":"eCollection","JCR":"Q1","JCRName":"BIOLOGY","Score":null,"Total":0}
引用次数: 0

Abstract

Cadmium can surpass fetal circulation and the blood-brain barrier due to its similar physicochemical properties to those of other divalent metals and causes diverse neuronal disorders. Previous reports have suggested a possible link between epigenetic alterations and neuronal changes in offspring due to cadmium exposure at different developmental stages. Hypermethylation of the glucocorticoid receptor NR3C1 disturbs the development of the hypothalamic-pituitary-adrenal axis, which in turn is responsible for the abnormal cognitive behavior of neonates. In addition, the upregulation of placental miR-509-3p and miR-193-5p expression was found to be the major cause of impaired development of the central nervous system. In this review, the epigenetic mechanism of cadmium-mediated neurotoxicity is described. Moreover, the journey of cadmium from the maternal body to the fetal body through circulation and to the neonatal body through breast milk is also tracked. The vulnerability of developing fetuses to cadmium is an alarming issue. Different types of epigenetic changes, such as DNA methylation, altered miRNA expression and histone modifications, are induced by cadmium and lead to various types of neurodevelopmental disorders. We hope this narrative review will provide distinct knowledge of the transportation of cadmium and its adverse effects on fetal neurodevelopment. See also the graphical abstract(Fig. 1).

Abstract Image

Abstract Image

Abstract Image

镉介导的产前至产后神经发育障碍的分子特征。
镉由于其与其他二价金属相似的物理化学性质,可以超越胎儿循环和血脑屏障,并引起多种神经系统疾病。以前的报告表明,由于镉暴露在不同发育阶段,后代的表观遗传改变和神经元变化之间可能存在联系。糖皮质激素受体NR3C1的高甲基化扰乱了下丘脑-垂体-肾上腺轴的发育,这反过来又导致了新生儿异常的认知行为。此外,胎盘miR-509-3p和miR-193-5p表达上调被发现是中枢神经系统发育受损的主要原因。本文就镉介导的神经毒性的表观遗传机制作一综述。此外,镉从母体通过循环进入胎儿体内,通过母乳进入新生儿体内的过程也被跟踪。发育中的胎儿对镉的脆弱性是一个令人担忧的问题。镉可诱导不同类型的表观遗传变化,如DNA甲基化、miRNA表达改变和组蛋白修饰,并导致各种类型的神经发育障碍。我们希望这篇叙述性综述将提供镉的运输及其对胎儿神经发育的不利影响的明确知识。另见图解摘要(图1)。1).
本文章由计算机程序翻译,如有差异,请以英文原文为准。
求助全文
约1分钟内获得全文 求助全文
来源期刊
EXCLI Journal
EXCLI Journal BIOLOGY-
CiteScore
8.00
自引率
2.20%
发文量
65
审稿时长
6-12 weeks
期刊介绍: EXCLI Journal publishes original research reports, authoritative reviews and case reports of experimental and clinical sciences. The journal is particularly keen to keep a broad view of science and technology, and therefore welcomes papers which bridge disciplines and may not suit the narrow specialism of other journals. Although the general emphasis is on biological sciences, studies from the following fields are explicitly encouraged (alphabetical order): aging research, behavioral sciences, biochemistry, cell biology, chemistry including analytical chemistry, clinical and preclinical studies, drug development, environmental health, ergonomics, forensic medicine, genetics, hepatology and gastroenterology, immunology, neurosciences, occupational medicine, oncology and cancer research, pharmacology, proteomics, psychiatric research, psychology, systems biology, toxicology
×
引用
GB/T 7714-2015
复制
MLA
复制
APA
复制
导出至
BibTeX EndNote RefMan NoteFirst NoteExpress
×
提示
您的信息不完整,为了账户安全,请先补充。
现在去补充
×
提示
您因"违规操作"
具体请查看互助需知
我知道了
×
提示
确定
请完成安全验证×
copy
已复制链接
快去分享给好友吧!
我知道了
右上角分享
点击右上角分享
0
联系我们:info@booksci.cn Book学术提供免费学术资源搜索服务,方便国内外学者检索中英文文献。致力于提供最便捷和优质的服务体验。 Copyright © 2023 布克学术 All rights reserved.
京ICP备2023020795号-1
ghs 京公网安备 11010802042870号
Book学术文献互助
Book学术文献互助群
群 号:604180095
Book学术官方微信