Article(id=1291753238374666998, tenantId=1146029695717560320, journalId=1291416913693474840, issueId=1291753151179280707, articleNumber=PA20260408_IEtdwnvi, orderNo=null, doi=10.3969/j.issn.1671-7856.2026.06.013, pmid=null, cstr=null, oa=null, hot=null, price=null, onlineType=0, articleFormat=0, articleType=null, articleTypeStr=null, receivedDate=1753977600000, receivedDateStr=2025-08-01, revisedDate=null, revisedDateStr=null, acceptedDate=null, acceptedDateStr=null, onlineDate=1785907571643, onlineDateStr=2026-08-05, pubDate=1774800000000, pubDateStr=2026-03-30, doiRegisterDate=null, doiRegisterDateStr=null, onlineIssueDate=1785907571643, onlineIssueDateStr=2026-08-05, onlineJustAcceptDate=null, onlineJustAcceptDateStr=null, onlineFirstDate=null, onlineFirstDateStr=null, sourceXml=null, magXml=null, createTime=1785907571643, creator=admin, updateTime=1785907571643, updator=admin, issue=Issue{id=1291753151179280707, tenantId=1146029695717560320, journalId=1291416913693474840, year='2026', volume='36', issue='6', pageStart='1', pageEnd='144', issueExtLink='null', onlineDate='null', pubDate='1774800000000', pubDateStr='2026-03-30', beforeIssueId=null, nextIssueId=null, price=null, status=1, issueComplete=1, articleOrder=1, issueType=1, specialIssue=null, createTime=1785907550854, creator='ztmeta', updateTime=1786331902788, updator='13701087609', preIssue=null, nextIssue=null, articleTotal=null, ext={EN=IssueExt(id=1293533012289941791, tenantId=1146029695717560320, journalId=1291416913693474840, issueId=1291753151179280707, language=EN, specialIssueTitle=, coverIllustrator=null, specialIssueEditor=, specialIssueAbout=), CN=IssueExt(id=1293533012289941792, tenantId=1146029695717560320, journalId=1291416913693474840, issueId=1291753151179280707, language=CN, specialIssueTitle=, coverIllustrator=null, specialIssueEditor=, specialIssueAbout=)}, issueFiles=null, downloadFileDto=null}, startPage=134, endPage=144, ext={EN=ArticleExt(id=1291753241373594360, articleId=1291753238374666998, tenantId=1146029695717560320, journalId=1291416913693474840, language=EN, title=Research progress on modeling and pathological mechanisms of diminished ovarian reserve, columnId=1292760404241969391, journalTitle=Chinese Journal of Comparative Medicine, columnName=Research Progress, runingTitle=null, highlight=null, articleAbstract=

We conducted a systematic review of the construction method and pathological mechanisms of animal and cellular models for diminished ovarian reserve (DOR), to provide a theoretical basis for understanding its pathophysiological mechanisms and references for future drug development and therapeutic strategies. We carried out extensive retrieval and analysis of the recent literature to identify the detailed diverse modeling approaches (including pharmaceutical induction, environmental factors, natural factors, and composite factors) and explored the roles of their mechanisms in DOR pathogenesis. The pathogenesis of DOR involves multiple factors, including oxidative stress, apoptosis and autophagy dysregulation, impaired angiogenesis, and imbalances in follicular development and the immune microenvironment. Studies also revealed intrinsic correlations among key signaling pathways in DOR models. Although existing DOR modeling method can effectively replicate Western medicine pathological features, models incorporating traditional Chinese medicine (TCM) syndrome characteristics remain scarce. Given the unique advantages of TCM in regulating the complex pathological network of DOR, future research is needed to prioritize the construction of TCM syndrome-oriented DOR models. This will support investigations into the scientific basis of TCM's multi-target regulatory mechanisms and provide a robust theoretical foundation for clinical applications.

, authors=Xinyue LI, Yi LIN, Ke NI, Ziyan XU, Yulu SHEN, Shengyang YANG, Qinhua ZHANG^*, authorsList=Xinyue LI, Yi LIN, Ke NI, Ziyan XU, Yulu SHEN, Shengyang YANG, Qinhua ZHANG, authorCompany=null, correspAuthors=Qinhua 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=1291753241293902583, articleId=1291753238374666998, tenantId=1146029695717560320, journalId=1291416913693474840, language=CN, title=卵巢储备功能减退模型制备及病理机制研究进展, columnId=1292760404409741552, journalTitle=中国比较医学杂志, columnName=研究进展, runingTitle=null, highlight=null, articleAbstract=

系统综述卵巢储备功能减退（DOR）模型的构建方式及其病理机制，为深入理解DOR的病理生理机制提供理论依据，并为未来相关药物开发及治疗策略的制定提供参考。广泛检索并分析近年来相关文献，详细梳理多种造模因素（包括药物诱导、环境因素、生物因素等）所构建的DOR模型方式，并深入探讨其病理机制在DOR发生发展中的作用。DOR的发病机制涉及氧化应激、细胞凋亡与自噬、血管生成障碍及卵泡发育与免疫微环境失衡等多种因素。研究还发现DOR模型中出现的相关通路之间存在内在关联性。现有DOR造模方法虽能高度模拟西医病理特征，但具备明确中医证候的“病证结合”模型极为匮乏。鉴于中医药在干预DOR复杂病理网络中展现出的多靶点调控优势，未来研究亟需构建高质量的病证结合DOR模型，并采用多维验证标准，以科学阐释中医药的整体调控机制，为DOR的诊治提供坚实理论基础。

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李欣悦（2002—），女，在读硕士研究生，研究方向：卵巢储备功能减退疾病。E-mail: 17805689876@163.com

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李欣悦（2002—），女，在读硕士研究生，研究方向：卵巢储备功能减退疾病。E-mail: 17805689876@163.com

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