Article(id=1292126494415938329, tenantId=1146029695717560320, journalId=1246415772164075586, issueId=1292126460546929080, articleNumber=null, orderNo=null, doi=10.13699/j.cnki.1001-6821.2026.03.020, pmid=null, cstr=null, oa=null, hot=null, price=null, onlineType=0, articleFormat=0, articleType=null, articleTypeStr=null, receivedDate=1763395200000, receivedDateStr=2025-11-18, revisedDate=null, revisedDateStr=null, acceptedDate=null, acceptedDateStr=null, onlineDate=1785996562818, onlineDateStr=2026-08-06, pubDate=1771257600000, pubDateStr=2026-02-17, doiRegisterDate=null, doiRegisterDateStr=null, onlineIssueDate=1785996562818, onlineIssueDateStr=2026-08-06, onlineJustAcceptDate=null, onlineJustAcceptDateStr=null, onlineFirstDate=null, onlineFirstDateStr=null, sourceXml=null, magXml=null, createTime=1785996562818, creator=13701087609, updateTime=1785996562818, updator=13701087609, issue=Issue{id=1292126460546929080, tenantId=1146029695717560320, journalId=1246415772164075586, year='2026', volume='42', issue='3', pageStart='301', pageEnd='450', issueExtLink='null', onlineDate='null', pubDate='1771257600000', pubDateStr='2026-02-17', beforeIssueId=null, nextIssueId=null, price=null, status=1, issueComplete=1, articleOrder=1, issueType=-1, specialIssue=null, createTime=1785996554742, creator='13701087609', updateTime=1786014541627, updator='13701087609', preIssue=null, nextIssue=null, articleTotal=null, ext={EN=IssueExt(id=1292201903060963536, tenantId=1146029695717560320, journalId=1246415772164075586, issueId=1292126460546929080, language=EN, specialIssueTitle=, coverIllustrator=null, specialIssueEditor=, specialIssueAbout=), CN=IssueExt(id=1292201903060963537, tenantId=1146029695717560320, journalId=1246415772164075586, issueId=1292126460546929080, language=CN, specialIssueTitle=, coverIllustrator=null, specialIssueEditor=, specialIssueAbout=)}, issueFiles=null, downloadFileDto=null}, startPage=427, endPage=433, ext={EN=ArticleExt(id=1292126494634042138, articleId=1292126494415938329, tenantId=1146029695717560320, journalId=1246415772164075586, language=EN, title=Advances in the effects and mechanisms of drugs and xenobiotics on bone development, columnId=1246531408630534361, journalTitle=Chinese Journal of Clinical Pharmacology, columnName=Review, runingTitle=null, highlight=null, articleAbstract=
Bone is not a static scaffold but a highly dynamic organ, whose development and homeostasis are significantly influenced by various drugs and xenobiotics. While traditional research has primarily focused on nutritional, hormonal, and genetic factors affecting bone, growing evidence highlights drugs and xenobiotics exposure as critical, non-negligible risk factors for bone health. This review systematically summarizes and analyzes the pharmacological impact of drugs (such as aromatase inhibitors, tyrosine kinase inhibitors, insulin sensitizers and antibiotics) and xenobiotics (such as heavy metals, environmental pollutants and endocrine disruptors) on bone development and metabolism. It emphasizes their roles in disrupting bone metabolic balance—through mechanisms including interference with signaling pathways, induction of oxidative stress, mimicry or antagonism of endocrine hormones, triggering of chronic inflammation, and induction of epigenetic alterations—leading to impaired bone microstructure, reduced bone strength, and increased fracture risk. Additionally, this review compiles potential bone-protective drugs and exogenous nutrients, evaluating their pharmacological actions in promoting bone health via supplemental osteogenic substrates, modulation of osteoblast/osteoclast activity, and repair of bone metabolic damage. The aim of this synthesis is to provide a pharmacological foundation for assessing risks posed by drugs and related xenobiotics to bone development and to offer new perspectives for preventing and treating bone-related disorders.
, authors=Li-ming CHONG
1, 2, Si-yu LIU
1, Yang YANG
1, Chi-yang ZHENG
1, Ting ZHANG
1, authorsList=Li-ming CHONG, Si-yu LIU, Yang YANG, Chi-yang ZHENG, Ting ZHANG, authorCompany=null, correspAuthors=Ting ZHANG, authorNote=null, correspAuthorsNote=null, copyrightStatement=null, copyrightOwner=null, extLink=null, articleAbsUrl=null, sourceXml=null, magXml=null, pdfUrl=null, pdf=null, pdfFileSize=null, pdfExtLink=null, richHtmlUrl=null, mobilePdfUrl=null, reviewReport=null, pdfFirstPage=null, abstractGraph=null, abstractGraphContent=null, abstractVideo=null, citation=null, cebUrl=null, magXmlContent=null, mapNumber=null, fund=null), CN=ArticleExt(id=1292126494885700379, articleId=1292126494415938329, tenantId=1146029695717560320, journalId=1246415772164075586, language=CN, title=药物及外源物质对骨骼发育的影响及机制研究现状, columnId=1246531408819278046, journalTitle=中国临床药理学杂志, columnName=综述, runingTitle=null, highlight=null, articleAbstract=
骨骼并非静态的支架,而是一个高度动态的器官,其发育与稳态维持受到多种药物和外源物质的显著影响。传统研究多聚焦于营养、激素和遗传因素对骨骼的影响,近年来越来越多的证据表明,药物及外源物质暴露是骨骼健康不可忽视的关键风险因素。本文系统综述了药物(如芳香化酶抑制剂、酪氨酸激酶抑制剂、胰岛素增敏剂和抗生素)及外源物质(如重金属、环境污染物和内分泌干扰物)对骨骼发育与代谢的药理影响,重点探讨其通过干扰信号通路、诱发氧化应激、模拟或拮抗内分泌激素、引发慢性炎症以及导致表观遗传改变等多种机制,干扰骨代谢平衡,导致骨微结构破坏、骨骼承受力强度下降和骨折风险增加。同时,本文还总结了具有骨保护潜力的药物及外源营养物质,分析其通过补充成骨原料、调节成骨/破骨细胞活性或修复骨代谢损伤等途径促进骨骼健康的作用。本综述旨在为评估药物及相关外源物质对骨骼发育的风险提供药理学依据,并为骨骼相关疾病的防治提供新思路。
, authors=崇立明
1, 2, 刘斯语
1, 杨阳
1, 郑驰阳
1, 张婷
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崇立明(1988-),男,硕士研究生,主要从事新药安全性评价方面的工作和研究
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1.NHC Key Lab of Reproduction Regulation, Shanghai Engineering Research Center of Reproductive Health Drug and Devices, Shanghai Institute for Biomedical and Pharmaceutical Technologies, Shanghai 200237, China
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2.厦门大学 生命科学学院,福建 厦门 361000, bio={"content":"
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1.国家卫生健康委生育调节药械重点实验室,上海生殖健康药具工程技术研究中心,上海市生物医药技术研究院,上海 200237, bio=null, bioImg=null, bioContent=null, aboutCorrespAuthor=null)}, companyList=[AuthorCompany(id=1292126495116387100, tenantId=1146029695717560320, journalId=1246415772164075586, articleId=1292126494415938329, xref=1., ext=[AuthorCompanyExt(id=1292126495124775709, tenantId=1146029695717560320, journalId=1246415772164075586, articleId=1292126494415938329, companyId=1292126495116387100, language=EN, country=null, province=null, city=null, postcode=null, companyName=null, departmentName=null, remark=
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