Article(id=1209139839723770391, tenantId=1146029695717560320, journalId=1189873630562394117, issueId=1209139833285505965, articleNumber=null, orderNo=null, doi=10.11855/j.issn.0577-7402.2021.07.12, pmid=null, cstr=null, oa=null, hot=null, price=null, onlineType=0, articleFormat=0, articleType=null, articleTypeStr=research-article, receivedDate=1608652800000, receivedDateStr=2020-12-23, revisedDate=1613318400000, revisedDateStr=2021-02-15, acceptedDate=null, acceptedDateStr=null, onlineDate=1766211002522, onlineDateStr=2025-12-20, pubDate=1627401600000, pubDateStr=2021-07-28, doiRegisterDate=null, doiRegisterDateStr=null, onlineIssueDate=1766211002522, onlineIssueDateStr=2025-12-20, onlineJustAcceptDate=null, onlineJustAcceptDateStr=null, onlineFirstDate=null, onlineFirstDateStr=null, sourceXml=null, magXml=null, createTime=1766211002522, creator=13701087609, updateTime=1766211002522, updator=13701087609, issue=Issue{id=1209139833285505965, tenantId=1146029695717560320, journalId=1189873630562394117, year='2021', volume='46', issue='7', pageStart='637', pageEnd='742', issueExtLink='null', onlineDate='null', pubDate='null', beforeIssueId=null, nextIssueId=null, price=null, status=1, issueComplete=1, articleOrder=1, issueType=-1, specialIssue=0, createTime=1766211000986, creator=13701087609, updateTime=1766212174313, updator=13701087609, preIssue=null, nextIssue=null, ext={EN=IssueExt(id=1209144754630168707, tenantId=1146029695717560320, journalId=1189873630562394117, issueId=1209139833285505965, language=EN, specialIssueTitle=, coverIllustrator=null, specialIssueEditor=, specialIssueAbout=), CN=IssueExt(id=1209144754630168708, tenantId=1146029695717560320, journalId=1189873630562394117, issueId=1209139833285505965, language=CN, specialIssueTitle=, coverIllustrator=null, specialIssueEditor=, specialIssueAbout=)}, issueFiles=null}, startPage=718, endPage=723, ext={EN=ArticleExt(id=1209139840008983076, articleId=1209139839723770391, tenantId=1146029695717560320, journalId=1189873630562394117, language=EN, title=Research progress on mitochondrial dysfunction of granulosa cells in polycystic ovary syndrome, columnId=1190243275882729994, journalTitle=Medical Journal of Chinese People’s Liberation Army, columnName=Review, runingTitle=null, highlight=null, articleAbstract=

Patients with polycystic ovary syndrome (PCOS) have impaired follicular development and maturation. Ovarian granulosa cells play an important regulatory role in the initiation, growth and development of primordial follicles, in which the mitochondria of granulosa cells are involved in the regulation of cell cycle, metabolism, and signal transduction, and provide energy support for oocyte meiosis, fertilization, and up to early embryonic development through energy metabolic pathways. Studying the mitochondrial function of granulosa cells is one of the best non-invasive methods to study the pathological mechanisms in PCOS patients and to evaluate oocyte quality and embryonic developmental potential. A large number of evidences have shown that PCOS is associated with mitochondrial dysfunction in ovarian granulosa cells by mechanisms including altered mitochondrial DNA(mtDNA) copy number and mutations in the mtDNA gene. Some studies have explored the improvement of mitochondrial function in PCOS granulosa cells to improve the impaired follicular development and maturation in PCOS. Therefore, the relevant research progress in recent years have been reviewed in present paper about mitochondrial dysfunction in PCOS granulosa cells, for exploring the mechanism of mitochondrial dysfunction in PCOS granulosa cells, and the ways and methods of improvement.

, correspAuthors=Chao-Qin Yu, authorNote=null, correspAuthorsNote=, 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, authorCompany=null, fund=null, authors=null, authorsList=Lin-Yi Song, Jin Yu, Chao-Qin Yu), CN=ArticleExt(id=1209139840453579315, articleId=1209139839723770391, tenantId=1146029695717560320, journalId=1189873630562394117, language=CN, title=多囊卵巢综合征颗粒细胞线粒体功能障碍的研究进展, columnId=1190243276029530637, journalTitle=解放军医学杂志, columnName=综述, runingTitle=null, highlight=null, articleAbstract=

多囊卵巢综合征(PCOS)患者存在卵泡发育和成熟障碍。卵巢颗粒细胞在原始卵泡的启动和生长发育过程中发挥着重要的调控作用，其中颗粒细胞的线粒体参与了细胞周期、代谢及信号转导等方面的调节，并通过能量代谢途径为卵母细胞减数分裂、受精直至早期胚胎发育提供能量支持。研究颗粒细胞的线粒体功能是探索PCOS的病理机制、评价卵母细胞质量和胚胎发育潜力的最佳无创性方法之一。大量证据显示，PCOS与卵巢颗粒细胞线粒体功能障碍相关，其机制包括线粒体DNA(mtDNA)拷贝数改变和mtDNA基因突变等。有研究从改善PCOS颗粒细胞的线粒体功能入手，对改善PCOS卵泡发育和成熟障碍进行了探索。该文对近年来PCOS颗粒细胞线粒体功能障碍的相关研究进展进行综述，以探讨PCOS颗粒细胞线粒体功能障碍的发生机制及其改善途径和方法。

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²Department of Gynecology of Traditional Chinese Medicine, the First Affiliated Hospital of Naval Medical University, Shanghai 200433, China, bio=null, bioImg=null, bioContent=null, aboutCorrespAuthor=null), CN=AuthorExt(id=1209139841959334496, tenantId=1146029695717560320, journalId=1189873630562394117, articleId=1209139839723770391, authorId=1209139841703481940, language=CN, stringName=宋琳奕, firstName=琳奕, middleName=null, lastName=宋, prefix=null, suffix=null, authorComment=null, nameInitials=null, affiliation=null, department=null, xref=^{1, 2}, address=¹中国科学院大学宁波华美医院中医科，浙江宁波 315000
²海军军医大学第一附属医院中医妇科，上海 200433, bio={"content":"

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