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Article(id=1248600566562181312, tenantId=1146029695717560320, journalId=1190317699101192196, issueId=1248600564427280576, articleNumber=1001-2494(2024)05-0385-07, orderNo=null, doi=null, pmid=null, cstr=null, oa=null, hot=null, price=null, onlineType=0, articleFormat=0, articleType=null, articleTypeStr=research-article, receivedDate=1697212800000, receivedDateStr=2023-10-14, revisedDate=null, revisedDateStr=null, acceptedDate=null, acceptedDateStr=null, onlineDate=1775619172943, onlineDateStr=2026-04-08, pubDate=1709827200000, pubDateStr=2024-03-08, doiRegisterDate=null, doiRegisterDateStr=null, onlineIssueDate=1775619172943, onlineIssueDateStr=2026-04-08, onlineJustAcceptDate=null, onlineJustAcceptDateStr=null, onlineFirstDate=null, onlineFirstDateStr=null, sourceXml=null, magXml=null, createTime=1775619172943, creator=13701087609, updateTime=1775619172943, updator=13701087609, issue=Issue{id=1248600564427280576, tenantId=1146029695717560320, journalId=1190317699101192196, year='2024', volume='59', issue='5', pageStart='377', pageEnd='468', issueExtLink='null', onlineDate='null', pubDate='null', beforeIssueId=null, nextIssueId=null, price=null, status=1, issueComplete=1, articleOrder=1, issueType=-1, specialIssue=null, createTime=1775619172436, creator=13701087609, updateTime=1775619904979, updator=13701087609, preIssue=null, nextIssue=null, ext={EN=IssueExt(id=1248603637019202091, tenantId=1146029695717560320, journalId=1190317699101192196, issueId=1248600564427280576, language=EN, specialIssueTitle=, coverIllustrator=null, specialIssueEditor=, specialIssueAbout=), CN=IssueExt(id=1248603637023396396, tenantId=1146029695717560320, journalId=1190317699101192196, issueId=1248600564427280576, language=CN, specialIssueTitle=, coverIllustrator=null, specialIssueEditor=, specialIssueAbout=)}, issueFiles=null}, startPage=385, endPage=391, ext={EN=ArticleExt(id=1248600566918697154, articleId=1248600566562181312, tenantId=1146029695717560320, journalId=1190317699101192196, language=EN, title=Research Progress of Compounds Inducing Cellular Mitophagy, columnId=null, journalTitle=Chinese Pharmaceutical Journal, columnName=null, runingTitle=null, highlight=null, articleAbstract=

Autophagy is a kind of programmed cell death that maintains metabolic and energetic homeostasis in organisms, which involves degradation of proteins, organelles, and other components. Mitophagy is a highly selective autophagy, which achieves its own metabolites and energy requirements by degrading excess or damaged mitochondria. Mitophagy plays an important role in the development of diseases, as one of selective autophagy most studied up to now. Some compounds have been found to induce mitophagy in cells through different mitochondrial signaling pathways, affecting the disease. In the current review, we summarized the mechanism of mitophagy induction and compounds that induce mitophagy are summarized, with the aim to provide a reference for the research and development of new drugs targeting mitochondria.

, correspAuthors=Qiongying HU, 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, authorCompany=null, fund=null, authors=null, authorsList=Ce CHEN, Kaikai JIN, Yuanyuan WEI, Qiongying HU), CN=ArticleExt(id=1248600568931963102, articleId=1248600566562181312, tenantId=1146029695717560320, journalId=1190317699101192196, language=CN, title=诱导细胞线粒体自噬化合物的研究进展, columnId=1190352408384471863, journalTitle=中国药学杂志, columnName=综述, runingTitle=null, highlight=null, articleAbstract=

自噬是一种特殊的程序性细胞死亡方式,维持着生物体内的重要代谢和能量平衡,该过程涉及降解蛋白质、细胞器等成分。线粒体自噬是一种高度选择性自噬,可通过降解多余或受损线粒体实现自身代谢物及能量需要。线粒体自噬作为如今选择性自噬中研究较多的领域,在疾病的发生发展中占有重要地位。研究发现一些化合物可通过不同的线粒体信号通路诱导细胞发生自噬,从而影响疾病的进程。作者描述了线粒体自噬的诱导机制,并就诱导细胞线粒体自噬化合物进行探讨,以期为开发靶向线粒体的治疗药物提供参考。

, correspAuthors=胡琼莹, authorNote=null, correspAuthorsNote=
*胡琼莹,女,博士,教授 研究方向:抗肿瘤、抗感染药物的发现及作用机制研究 Tel:(0576)88665198
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陈策和金锴凯为共同第一作者

陈策,女,硕士研究生 研究方向:临床药学;

金锴凯,女,学士 研究方向:药理学。

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金锴凯,女,学士 研究方向:药理学。

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金锴凯,女,学士 研究方向:药理学。

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The nuclear receptor 4A family members: mediators in human disease and autophagy[J]. Cell Mol Biol Lett, 2020, 25(1):48. DOI 10.1186/s11658-020-00241-w., articleTitle=The nuclear receptor 4A family members: mediators in human disease and autophagy, refAbstract=null), Reference(id=1248712174923858170, tenantId=1146029695717560320, journalId=1190317699101192196, articleId=1248600566562181312, doi=null, pmid=null, pmcid=null, year=2018, volume=217, issue=3, pageStart=813, pageEnd=822, url=null, language=null, rfNumber=[2], rfOrder=1, authorNames=CADWELL K, DEBNATH J, journalName=J Cell Biol, refType=null, unstructuredReference=CADWELL K, DEBNATH J. Beyond self-eating: the control of nonautophagic functions and signaling pathways by autophagy-related proteins[J]. J Cell Biol, 2018, 217(3): 813-822., articleTitle=Beyond self-eating: the control of nonautophagic functions and signaling pathways by autophagy-related proteins, refAbstract=null), Reference(id=1248712175003549949, tenantId=1146029695717560320, journalId=1190317699101192196, articleId=1248600566562181312, doi=null, pmid=null, pmcid=null, year=2007, volume=462, issue=2, pageStart=245, pageEnd=253, url=null, language=null, rfNumber=[3], rfOrder=2, authorNames=KIM I, RODRIGUEZ-ENRIQUEZ S, LEMASTERS J J, journalName=Arch Biochem Biophy, refType=null, unstructuredReference=KIM I, RODRIGUEZ-ENRIQUEZ S, LEMASTERS J J. Selective degradation of mitochondria by mitophagy[J]. Arch Biochem Biophy, 2007, 462(2): 245-253., articleTitle=Selective degradation of mitochondria by mitophagy, refAbstract=null), Reference(id=1248712175095824641, tenantId=1146029695717560320, journalId=1190317699101192196, articleId=1248600566562181312, doi=null, pmid=null, pmcid=null, year=2021, volume=11, issue=1, pageStart=38, pageEnd=null, url=null, language=null, rfNumber=[4], rfOrder=3, authorNames=CHOUBEY V, ZEB A, KAASIK A, journalName=Cells, refType=null, unstructuredReference=CHOUBEY V, ZEB A, KAASIK A. Molecular mechanisms and regulation of mammalian mitophagy[J]. Cells, 2021, 11(1):38. DOI: 10.3390/cells11010038., articleTitle=Molecular mechanisms and regulation of mammalian mitophagy, refAbstract=null), Reference(id=1248712175179710725, tenantId=1146029695717560320, journalId=1190317699101192196, articleId=1248600566562181312, doi=null, pmid=null, pmcid=null, year=2021, volume=17, issue=2, pageStart=385, pageEnd=401, url=null, language=null, rfNumber=[5], rfOrder=4, authorNames=YAO R Q, REN C, XIA Z F, journalName=Autophagy, refType=null, unstructuredReference=YAO R Q, REN C, XIA Z F, et al. Organelle-specific autophagy in inflammatory diseases: a potential therapeutic target underlying the quality control of multiple organelles[J]. Autophagy, 2021, 17(2): 385-401., articleTitle=Organelle-specific autophagy in inflammatory diseases: a potential therapeutic target underlying the quality control of multiple organelles, refAbstract=null), Reference(id=1248712175255208200, tenantId=1146029695717560320, journalId=1190317699101192196, articleId=1248600566562181312, doi=null, pmid=null, pmcid=null, year=2016, volume=26, issue=10, pageStart=733, pageEnd=744, url=null, language=null, rfNumber=[6], rfOrder=5, authorNames=NGUYEN T N, PADMAN B S, LAZAROU M, journalName=Trends Cell Biol, refType=null, unstructuredReference=NGUYEN T N, PADMAN B S, LAZAROU M. Deciphering the molecular signals of PINK1/Parkin mitophagy[J]. Trends Cell Biol, 2016, 26(10): 733-744., articleTitle=Deciphering the molecular signals of PINK1/Parkin mitophagy, refAbstract=null), Reference(id=1248712175343288587, tenantId=1146029695717560320, journalId=1190317699101192196, articleId=1248600566562181312, doi=null, pmid=null, pmcid=null, year=2021, volume=40, issue=3, pageStart=e104705, pageEnd=null, url=null, language=null, rfNumber=[7], rfOrder=6, authorNames=ONISHI M, YAMANO K, SATO M, journalName=The EMBO J, refType=null, unstructuredReference=ONISHI M, YAMANO K, SATO M, et al. Molecular mechanisms and physiological functions of mitophagy[J]. The EMBO J, 2021, 40(3): e104705. DOI: 10.15252/embj.2020104705., articleTitle=Molecular mechanisms and physiological functions of mitophagy, refAbstract=null), Reference(id=1248712175410397453, tenantId=1146029695717560320, journalId=1190317699101192196, articleId=1248600566562181312, doi=null, pmid=null, pmcid=null, year=2011, volume=27, issue=4, pageStart=455, pageEnd=458, url=null, language=null, rfNumber=[8], rfOrder=7, authorNames=LIU C L, HE K L, WANG L L, journalName=Chin Pharmacol Bull, refType=null, unstructuredReference=LIU C L, HE K L, WANG L L. Research progress of cell protection strategy based on endoplasmic reticulum stress pathway[J]. Chin Pharmacol Bull (中国药理学通报), 2011, 27(4): 455-458., articleTitle=Research progress of cell protection strategy based on endoplasmic reticulum stress pathway, refAbstract=null), Reference(id=1248712175502672146, tenantId=1146029695717560320, journalId=1190317699101192196, articleId=1248600566562181312, doi=null, pmid=null, pmcid=null, year=2007, volume=25, issue=2, pageStart=193, pageEnd=205, url=null, language=null, rfNumber=[9], rfOrder=8, authorNames=HØYER-HANSEN M, BASTHOLM L, SZYNIAROWSKI P, journalName=Mol Cell, refType=null, unstructuredReference=HØYER-HANSEN M, BASTHOLM L, SZYNIAROWSKI P, et al. Control of macroautophagy by calcium, calmodulin-dependent kinase kinase-beta, and Bcl-2[J]. Mol Cell, 2007, 25(2): 193-205., articleTitle=Control of macroautophagy by calcium, calmodulin-dependent kinase kinase-beta, and Bcl-2, refAbstract=null), Reference(id=1248712175590752530, tenantId=1146029695717560320, journalId=1190317699101192196, articleId=1248600566562181312, doi=null, pmid=null, pmcid=null, year=2012, volume=8, issue=9, pageStart=1312, pageEnd=1324, url=null, language=null, rfNumber=[10], rfOrder=9, authorNames=RUBIO N, COUPIENNE I, DI VALENTIN E, journalName=Autophagy, refType=null, unstructuredReference=RUBIO N, COUPIENNE I, DI VALENTIN E, et al. Spatiotemporal autophagic degradation of oxidatively damaged organelles after photodynamic stress is amplified by mitochondrial reactive oxygen species[J]. Autophagy, 2012, 8(9): 1312-1324., articleTitle=Spatiotemporal autophagic degradation of oxidatively damaged organelles after photodynamic stress is amplified by mitochondrial reactive oxygen species, refAbstract=null), Reference(id=1248712175666250005, tenantId=1146029695717560320, journalId=1190317699101192196, articleId=1248600566562181312, doi=null, pmid=null, pmcid=null, year=2020, volume=432, issue=1, pageStart=231, pageEnd=239, url=null, language=null, rfNumber=[11], rfOrder=10, authorNames=PAPADOPOULOS C, KRAVIC B, MEYER H, journalName=J Mol Biol, refType=null, unstructuredReference=PAPADOPOULOS C, KRAVIC B, MEYER H. Repair or lysophagy: dealing with damaged lysosomes[J]. J Mol Biol, 2020, 432(1): 231-239., articleTitle=Repair or lysophagy: dealing with damaged lysosomes, refAbstract=null), Reference(id=1248712175733358871, tenantId=1146029695717560320, journalId=1190317699101192196, articleId=1248600566562181312, doi=null, pmid=null, pmcid=null, year=2014, volume=10, issue=2, pageStart=133, pageEnd=140, url=null, language=null, rfNumber=[12], rfOrder=11, authorNames=WANG W J, WANG Y, CHEN H Z, journalName=Nat Chem Biol, refType=null, unstructuredReference=WANG W J, WANG Y, CHEN H Z, et al. Orphan nuclear receptor TR3 acts in autophagic cell death via mitochondrial signaling pathway[J]. Nat Chem Biol, 2014, 10(2): 133-140., articleTitle=Orphan nuclear receptor TR3 acts in autophagic cell death via mitochondrial signaling pathway, refAbstract=null), Reference(id=1248712175821439259, tenantId=1146029695717560320, journalId=1190317699101192196, articleId=1248600566562181312, doi=null, pmid=null, pmcid=null, year=2017, volume=66, issue=1, pageStart=141, pageEnd=53, url=null, language=null, rfNumber=[13], rfOrder=12, authorNames=HU M, LUO Q, ALITONGBIEKE G, journalName=Mol Cell, refType=null, unstructuredReference=HU M, LUO Q, ALITONGBIEKE G, et al. Celastrol-Induced Nur77 Interaction with TRAF2 Alleviates Inflammation by Promoting Mitochondrial Ubiquitination and Autophagy[J]. Mol Cell, 2017, 66(1): 141-53.e6., articleTitle=Celastrol-Induced Nur77 Interaction with TRAF2 Alleviates Inflammation by Promoting Mitochondrial Ubiquitination and Autophagy, refAbstract=null), Reference(id=1248712175892742428, tenantId=1146029695717560320, journalId=1190317699101192196, articleId=1248600566562181312, doi=null, pmid=null, pmcid=null, year=2021, volume=22, issue=11, pageStart=5820, pageEnd=null, url=null, language=null, rfNumber=[14], rfOrder=13, authorNames=ZENG C, ZOU T, QU J, journalName=Int J Mol Sci, refType=null, unstructuredReference=ZENG C, ZOU T, QU J, et al. Cyclovirobuxine D induced-mitophagy through the p65/BNIP3/LC3 axis potentiates its apoptosis-inducing effects in lung cancer cells[J]. Int J Mol Sci, 2021, 22(11):5820. DOI: 10.3390/ijms22115820., articleTitle=Cyclovirobuxine D induced-mitophagy through the p65/BNIP3/LC3 axis potentiates its apoptosis-inducing effects in lung cancer cells, refAbstract=null), Reference(id=1248712175989211423, tenantId=1146029695717560320, journalId=1190317699101192196, articleId=1248600566562181312, doi=null, pmid=null, pmcid=null, year=2019, volume=67, issue=36, pageStart=10097, pageEnd=10106, url=null, language=null, rfNumber=[15], rfOrder=14, authorNames=WANG W, WANG M, RUAN Y, journalName=J Agric Food Chem, refType=null, unstructuredReference=WANG W, WANG M, RUAN Y, et al. Ginkgolic acids impair mitochondrial function by decreasing mitochondrial biogenesis and promoting FUNDC1-dependent mitophagy[J]. J Agric Food Chem, 2019, 67(36): 10097-10106., articleTitle=Ginkgolic acids impair mitochondrial function by decreasing mitochondrial biogenesis and promoting FUNDC1-dependent mitophagy, refAbstract=null), Reference(id=1248712176064708895, tenantId=1146029695717560320, journalId=1190317699101192196, articleId=1248600566562181312, doi=null, pmid=null, pmcid=null, year=2020, volume=34, issue=7, pageStart=1659, pageEnd=1669, url=null, language=null, rfNumber=[16], rfOrder=15, authorNames=HOU J, YUN Y, XUE J, journalName=Phytother Res, refType=null, unstructuredReference=HOU J, YUN Y, XUE J, et al. Doxorubicin-induced normal breast epithelial cellular aging and its related breast cancer growth through mitochondrial autophagy and oxidative stress mitigated by ginsenoside Rh2[J]. Phytother Res, 2020, 34(7): 1659-1669., articleTitle=Doxorubicin-induced normal breast epithelial cellular aging and its related breast cancer growth through mitochondrial autophagy and oxidative stress mitigated by ginsenoside Rh2, refAbstract=null), Reference(id=1248712176127623457, tenantId=1146029695717560320, journalId=1190317699101192196, articleId=1248600566562181312, doi=null, pmid=null, pmcid=null, year=2019, volume=99, issue=6, pageStart=819, pageEnd=829, url=null, language=null, rfNumber=[17], rfOrder=16, authorNames=LI T, LIU Y, XU W, journalName=Lab Invest, refType=null, unstructuredReference=LI T, LIU Y, XU W, et al. Polydatin mediates Parkin-dependent mitophagy and protects against mitochondria-dependent apoptosis in acute respiratory distress syndrome[J]. Lab Invest, 2019, 99(6): 819-829., articleTitle=Polydatin mediates Parkin-dependent mitophagy and protects against mitochondria-dependent apoptosis in acute respiratory distress syndrome, refAbstract=null), Reference(id=1248712176253452579, tenantId=1146029695717560320, journalId=1190317699101192196, articleId=1248600566562181312, doi=null, pmid=null, pmcid=null, year=2020, volume=177, issue=null, pageStart=113997, pageEnd=null, url=null, language=null, rfNumber=[18], rfOrder=17, authorNames=GAO Y, LI J, LI J, journalName=Biochem Pharmacol, refType=null, unstructuredReference=GAO Y, LI J, LI J, et al. Tetrahydroxy stilbene glycoside alleviated inflammatory damage by mitophagy via AMPK related PINK1/Parkin signaling pathway[J]. Biochem Pharmacol, 2020, 177: 113997. DOI: 10.1016/j.bcp.2020.113997., articleTitle=Tetrahydroxy stilbene glycoside alleviated inflammatory damage by mitophagy via AMPK related PINK1/Parkin signaling pathway, refAbstract=null), Reference(id=1248712176316367143, tenantId=1146029695717560320, journalId=1190317699101192196, articleId=1248600566562181312, doi=null, pmid=null, pmcid=null, year=2021, volume=26, issue=10, pageStart=2858, pageEnd=null, url=null, language=null, rfNumber=[19], rfOrder=18, authorNames=FENG J, MANSOURIPOUR A, XI Z, journalName=Switzerland), refType=null, unstructuredReference=FENG J, MANSOURIPOUR A, XI Z, et al. Nujiangexanthone A inhibits cervical cancer cell proliferation by promoting mitophagy[J]. Molecules (Basel, Switzerland), 2021, 26(10):2858. DOI: 10.3390/molecules26102858., articleTitle=Nujiangexanthone A inhibits cervical cancer cell proliferation by promoting mitophagy, refAbstract=null), Reference(id=1248712176396058922, tenantId=1146029695717560320, journalId=1190317699101192196, articleId=1248600566562181312, doi=null, pmid=null, pmcid=null, year=2018, volume=19, issue=null, pageStart=263, pageEnd=273, url=null, language=null, rfNumber=[20], rfOrder=19, authorNames=ZHANG J, SUN X, WANG L, journalName=Redox Biol, refType=null, unstructuredReference=ZHANG J, SUN X, WANG L, et al. Artesunate-induced mitophagy alters cellular redox status[J]. Redox Biol, 2018, 19: 263-273., articleTitle=Artesunate-induced mitophagy alters cellular redox status, refAbstract=null), Reference(id=1248712176467362093, tenantId=1146029695717560320, journalId=1190317699101192196, articleId=1248600566562181312, doi=null, pmid=null, pmcid=null, year=2022, volume=21, issue=8, pageStart=e13662, pageEnd=null, url=null, language=null, rfNumber=[21], rfOrder=20, authorNames=D'AMICO D, OLMER M, FOUASSIER A M, journalName=Aging Cell, refType=null, unstructuredReference=D'AMICO D, OLMER M, FOUASSIER A M, et al. Urolithin A improves mitochondrial health, reduces cartilage degeneration, and alleviates pain in osteoarthritis[J]. Aging Cell, 2022, 21(8): e13662. DOI: 10.1111/acel.13662., articleTitle=Urolithin A improves mitochondrial health, reduces cartilage degeneration, and alleviates pain in osteoarthritis, refAbstract=null), Reference(id=1248712176538665263, tenantId=1146029695717560320, journalId=1190317699101192196, articleId=1248600566562181312, doi=null, pmid=null, pmcid=null, year=2016, volume=6, issue=null, pageStart=34403, pageEnd=null, url=null, language=null, rfNumber=[22], rfOrder=21, authorNames=GAO H, CHEN Z, FU Y, journalName=Sci Rep, refType=null, unstructuredReference=GAO H, CHEN Z, FU Y, et al. Nur77 exacerbates PC12 cellular injury in vitro by aggravating mitochondrial impairment and endoplasmic reticulum stress[J]. Sci Rep, 2016, 6: 34403. DOI: 10.1038/srep34403., articleTitle=Nur77 exacerbates PC12 cellular injury in vitro by aggravating mitochondrial impairment and endoplasmic reticulum stress, refAbstract=null), Reference(id=1248712176635134256, tenantId=1146029695717560320, journalId=1190317699101192196, articleId=1248600566562181312, doi=null, pmid=null, pmcid=null, year=2021, volume=190, issue=null, pageStart=114588, pageEnd=null, url=null, language=null, rfNumber=[23], rfOrder=22, authorNames=SUN H, OU T, HU J, journalName=Biochem Pharmacol, refType=null, unstructuredReference=SUN H, OU T, HU J, et al. Nitazoxanide impairs mitophagy flux through ROS-mediated mitophagy initiation and lysosomal dysfunction in bladder cancer[J]. Biochem Pharmacol, 2021, 190: 114588. DOI: 10.1016/j.bcp.2021.114588., articleTitle=Nitazoxanide impairs mitophagy flux through ROS-mediated mitophagy initiation and lysosomal dysfunction in bladder cancer, refAbstract=null), Reference(id=1248712176714826036, tenantId=1146029695717560320, journalId=1190317699101192196, articleId=1248600566562181312, doi=null, pmid=null, pmcid=null, year=2008, volume=4, issue=9, pageStart=548, pageEnd=556, url=null, language=null, rfNumber=[24], rfOrder=23, authorNames=ZHAN Y, DU X, CHEN H, journalName=Nat Chem Biol, refType=null, unstructuredReference=ZHAN Y, DU X, CHEN H, et al. Cytosporone B is an agonist for nuclear orphan receptor Nur77[J]. Nat Chem Biol, 2008, 4(9): 548-556., articleTitle=Cytosporone B is an agonist for nuclear orphan receptor Nur77, refAbstract=null), Reference(id=1248712176781934899, tenantId=1146029695717560320, journalId=1190317699101192196, articleId=1248600566562181312, doi=null, pmid=null, pmcid=null, year=2018, volume=53, issue=7, pageStart=513, pageEnd=517, url=null, language=null, rfNumber=[25], rfOrder=24, authorNames=LI N, ZHANG T D, WANG Y F, journalName=中国药学杂志, refType=null, unstructuredReference=LI N, ZHANG T D, WANG Y F, et al. Autophagy of human HeLa cells induced by tripterine in vitro and in vivo and its molecular mechanism[J]. Chin Pharm J(中国药学杂志), 2018, 53(7): 513-517., articleTitle=Autophagy of human HeLa cells induced by tripterine in vitro and in vivo and its molecular mechanism, refAbstract=null), Reference(id=1248712176857432373, tenantId=1146029695717560320, journalId=1190317699101192196, articleId=1248600566562181312, doi=null, pmid=null, pmcid=null, year=2018, volume=15, issue=5, pageStart=6400, pageEnd=6408, url=null, language=null, rfNumber=[26], rfOrder=25, authorNames=QI Q M, XUE Y C, LV J, journalName=Oncol Lett, refType=null, unstructuredReference=QI Q M, XUE Y C, LV J, et al. Ginkgolic acids induce HepG2 cell death via a combination of apoptosis, autophagy and the mitochondrial pathway[J]. Oncol Lett, 2018, 15(5): 6400-6408., articleTitle=Ginkgolic acids induce HepG2 cell death via a combination of apoptosis, autophagy and the mitochondrial pathway, refAbstract=null), Reference(id=1248712178409324855, tenantId=1146029695717560320, journalId=1190317699101192196, articleId=1248600566562181312, doi=null, pmid=null, pmcid=null, year=2014, volume=59, issue=9, pageStart=1412, pageEnd=1421, url=null, language=null, rfNumber=[27], rfOrder=26, authorNames=LI T, CAI S, ZENG Z, journalName=Respir Care, refType=null, unstructuredReference=LI T, CAI S, ZENG Z, et al. Protective effect of polydatin against burn-induced lung injury in rats[J]. Respir Care, 2014, 59(9): 1412-1421., articleTitle=Protective effect of polydatin against burn-induced lung injury in rats, refAbstract=null), Reference(id=1248712178497405241, tenantId=1146029695717560320, journalId=1190317699101192196, articleId=1248600566562181312, doi=null, pmid=null, pmcid=null, year=2020, volume=247, issue=null, pageStart=112232, pageEnd=null, url=null, language=null, rfNumber=[28], rfOrder=27, authorNames=LI F, ZHANG T, HE Y, journalName=J Ethnopharmacol, refType=null, unstructuredReference=LI F, ZHANG T, HE Y, et al. Inflammation inhibition and gut microbiota regulation by TSG to combat atherosclerosis in ApoE(-/-) mice[J]. J Ethnopharmacol, 2020, 247: 112232. DOI: 10.1016/j.jep.2019.112232., articleTitle=Inflammation inhibition and gut microbiota regulation by TSG to combat atherosclerosis in ApoE(-/-) mice, refAbstract=null), Reference(id=1248712178572902715, tenantId=1146029695717560320, journalId=1190317699101192196, articleId=1248600566562181312, doi=null, pmid=null, pmcid=null, year=2021, volume=27, issue=7, pageStart=687, pageEnd=699, url=null, language=null, rfNumber=[29], rfOrder=28, authorNames=D'AMICO D, ANDREUX P A, VALDÉS P, journalName=null, refType=null, unstructuredReference=D'AMICO D, ANDREUX P A, VALDÉS P, et al. Impact of the natural compound urolithin A on health, disease, and aging [J]. Trends Mol Med, 2021, 27(7): 687-699., articleTitle=Impact of the natural compound urolithin A on health, disease, and aging [J]. Trends Mol Med, refAbstract=null), Reference(id=1248712178640011582, tenantId=1146029695717560320, journalId=1190317699101192196, articleId=1248600566562181312, doi=null, pmid=null, pmcid=null, year=2021, volume=41, issue=7, pageStart=876, pageEnd=883, url=null, language=null, rfNumber=[30], rfOrder=29, authorNames=YUAN X, YE Y, XUE Z, journalName=上海交通大学学报医学版, refType=null, unstructuredReference=YUAN X, YE Y, XUE Z. 6-OHDA-induced Parkinson's disease mice showed a senescence phenotype characterized by up-regulation of p16-(Ink4a) and astrocyte senescence[J]. J Shanghai Jiao Tong Univ(Med Ed)(上海交通大学学报医学版), 2021, 41(7): 876-883., articleTitle=6-OHDA-induced Parkinson's disease mice showed a senescence phenotype characterized by up-regulation of p16-(Ink4a) and astrocyte senescence, refAbstract=null), Reference(id=1248712178723897666, tenantId=1146029695717560320, journalId=1190317699101192196, articleId=1248600566562181312, doi=null, pmid=null, pmcid=null, year=2014, volume=110, issue=null, pageStart=94, pageEnd=103, url=null, language=null, rfNumber=[31], rfOrder=30, authorNames=ROSSIGNOL J F, journalName=Antiviral Res, refType=null, unstructuredReference=ROSSIGNOL J F. Nitazoxanide: a first-in-class broad-spectrum antiviral agent[J]. Antiviral Res, 2014, 110: 94-103., articleTitle=Nitazoxanide: a first-in-class broad-spectrum antiviral agent, refAbstract=null), Reference(id=1248712178820366661, tenantId=1146029695717560320, journalId=1190317699101192196, articleId=1248600566562181312, doi=null, pmid=null, pmcid=null, year=2013, volume=494, issue=7436, pageStart=201, pageEnd=206, url=null, language=null, rfNumber=[32], rfOrder=31, authorNames=SHOJI-KAWATA S, SUMPTER R, LEVENO M, journalName=Nature, refType=null, unstructuredReference=SHOJI-KAWATA S, SUMPTER R, LEVENO M, et al. Identification of a candidate therapeutic autophagy-inducing peptide[J]. 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自噬的基本过程可分为5步:①自噬诱导信号的启动,②隔离吞噬体形成,③包裹货物的双层膜结构的延伸和封闭以形成自噬体,④自噬体与溶酶体的对接融合,⑤溶酶体酶降解自噬空泡内容物。

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THPN-1-(3,4,5-三羟基苯基)壬-1-酮;Celastrol-雷公藤红素;CVB-D-环维黄杨星D;GA-银杏酸;PD-白藜芦醇苷;TSG-二苯乙烯苷; NJXA-Nujiangexanthone A;ART-青蒿琥酯;UA-尿石素A;6-OHDA- 6-羟基多巴胺; NTZ -硝唑尼特。

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项目 线粒体自噬 内质网自噬 溶酶体自噬
类别 受损或衰老的线粒体 受损或衰老的内质网 受损或衰老的溶酶体
条件 营养缺乏缺氧 营养缺乏内质网应激 营养缺乏
受体 OPTN,p62,Fis1,BNIP3L/NIX、BNIP3、FUNDC1,PHB2,CL等 FAM134B,SEC62,RTN3,ATL3等 p62
途径 PINK1/Parkin通路;BNIP3L/NIX、BNIP3、FUNDC1等受体
介导通路		 ERN1/EIF2AK3/ATF6通路;Ca2+
依赖的AMPK/mTOR通路		 Gal3/TRIM16/ULK1通路;Gal8/NDP52/LC3通路
代谢产物 磷脂、氨基酸、单糖、核苷酸和其他小分子物质 磷脂、氨基酸、单糖、核苷酸和其他小分子物质 磷脂、氨基酸、单糖、核苷酸和其他小分子物质
), ArticleFig(id=1248712174282129635, tenantId=1146029695717560320, journalId=1190317699101192196, articleId=1248600566562181312, language=CN, label=表1, caption=

线粒体、内质网、溶酶体介导自噬的差异

, figureFileSmall=null, figureFileBig=null, tableContent=
项目 线粒体自噬 内质网自噬 溶酶体自噬
类别 受损或衰老的线粒体 受损或衰老的内质网 受损或衰老的溶酶体
条件 营养缺乏缺氧 营养缺乏内质网应激 营养缺乏
受体 OPTN,p62,Fis1,BNIP3L/NIX、BNIP3、FUNDC1,PHB2,CL等 FAM134B,SEC62,RTN3,ATL3等 p62
途径 PINK1/Parkin通路;BNIP3L/NIX、BNIP3、FUNDC1等受体
介导通路		 ERN1/EIF2AK3/ATF6通路;Ca2+
依赖的AMPK/mTOR通路		 Gal3/TRIM16/ULK1通路;Gal8/NDP52/LC3通路
代谢产物 磷脂、氨基酸、单糖、核苷酸和其他小分子物质 磷脂、氨基酸、单糖、核苷酸和其他小分子物质 磷脂、氨基酸、单糖、核苷酸和其他小分子物质
), ArticleFig(id=1248712174378598630, tenantId=1146029695717560320, journalId=1190317699101192196, articleId=1248600566562181312, language=EN, label=null, caption=null, figureFileSmall=null, figureFileBig=null, tableContent=
化合物 信号通路 作用细胞系 给药浓度 作用时间 文献
1-(3,4,5-三羟
基苯基)壬-1-酮(THPN)		 Nur77/NIX/ANT1-VDAC1通路 黑色素瘤细胞 20 μmol·L-1 24 h [12]
雷公藤红素(Celastrol) Nur77/TRAF2/p62通路 肝癌细胞 4 μmol·L-1 1 h [13]
环维黄杨星D(CVB-D) p65/BNIP3/LC3通路 肺癌细胞 30 μmol·L-1 24 h [14]
银杏酸(GA) FUNDC1依赖性通路 宫颈癌细胞HeLa细胞 50 μmol·L-1 24 h [15]
人参皂苷Rh2 PINK1/Parkin通路 乳腺癌细胞MCF-7 20 μg·mL-1 9 d [16]
白藜芦醇苷(PD) Parkin依赖性通路 脂多糖处理的人正常肺上皮
细胞BEAS-2B细胞		 50 μmol·L-1 6 h [17]
二苯乙烯苷(TSG) AMPK/PINK1/Parkin通路 小鼠原代小胶质细胞 10, 1 μmol·L-1、100 nmol·L-1 24 h [18]
Nujiangexanthone A(NJXA) PINK1/Parkin/p62通路 宫颈癌细胞HeLa细胞 20 μmol·L-1 4 h [19]
青蒿琥酯(ART)
尿石素A(UA)		 PINK1/Parkin通路
PINK1/Parkin/泛素通路		 宫颈癌细胞HeLa细胞人软骨
细胞		 10、6.25、12 μmol·L-1 12、24 h [20-21]
6-羟基多巴胺(6-OHDA) Nur77/PINK1/Parkin通路 嗜铬细胞瘤细胞PC12 100 μmol·L-1 24 h [22]
硝唑尼特(NTZ) PINK1/OPTN/NDP52通路 膀胱癌细胞 60 μmol·L-1 24 h [23]
), ArticleFig(id=1248712174470873322, tenantId=1146029695717560320, journalId=1190317699101192196, articleId=1248600566562181312, language=CN, label=表2, caption=

诱导细胞线粒体自噬的化合物及信号通路

, figureFileSmall=null, figureFileBig=null, tableContent=
化合物 信号通路 作用细胞系 给药浓度 作用时间 文献
1-(3,4,5-三羟
基苯基)壬-1-酮(THPN)		 Nur77/NIX/ANT1-VDAC1通路 黑色素瘤细胞 20 μmol·L-1 24 h [12]
雷公藤红素(Celastrol) Nur77/TRAF2/p62通路 肝癌细胞 4 μmol·L-1 1 h [13]
环维黄杨星D(CVB-D) p65/BNIP3/LC3通路 肺癌细胞 30 μmol·L-1 24 h [14]
银杏酸(GA) FUNDC1依赖性通路 宫颈癌细胞HeLa细胞 50 μmol·L-1 24 h [15]
人参皂苷Rh2 PINK1/Parkin通路 乳腺癌细胞MCF-7 20 μg·mL-1 9 d [16]
白藜芦醇苷(PD) Parkin依赖性通路 脂多糖处理的人正常肺上皮
细胞BEAS-2B细胞		 50 μmol·L-1 6 h [17]
二苯乙烯苷(TSG) AMPK/PINK1/Parkin通路 小鼠原代小胶质细胞 10, 1 μmol·L-1、100 nmol·L-1 24 h [18]
Nujiangexanthone A(NJXA) PINK1/Parkin/p62通路 宫颈癌细胞HeLa细胞 20 μmol·L-1 4 h [19]
青蒿琥酯(ART)
尿石素A(UA)		 PINK1/Parkin通路
PINK1/Parkin/泛素通路		 宫颈癌细胞HeLa细胞人软骨
细胞		 10、6.25、12 μmol·L-1 12、24 h [20-21]
6-羟基多巴胺(6-OHDA) Nur77/PINK1/Parkin通路 嗜铬细胞瘤细胞PC12 100 μmol·L-1 24 h [22]
硝唑尼特(NTZ) PINK1/OPTN/NDP52通路 膀胱癌细胞 60 μmol·L-1 24 h [23]
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诱导细胞线粒体自噬化合物的研究进展
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陈策 1, 2 , 金锴凯 1 , 魏园园 1 , 胡琼莹 1, 2, *
中国药学杂志 | 综述 2024,59(5): 385-391
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中国药学杂志 | 综述 2024, 59(5): 385-391
诱导细胞线粒体自噬化合物的研究进展
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陈策1, 2, 金锴凯1, 魏园园1, 胡琼莹1, 2, *
作者信息
  • 1 温岭市第一人民医院(台州学院附属温岭医院), 台州学院医学院, 浙江 台州 318000
  • 2 河北北方学院药学院, 河北省神经药理学重点实验室, 河北 张家口 075000

    • 陈策,女,硕士研究生 研究方向:临床药学;

    金锴凯,女,学士 研究方向:药理学。

通讯作者:

*胡琼莹,女,博士,教授 研究方向:抗肿瘤、抗感染药物的发现及作用机制研究 Tel:(0576)88665198
Research Progress of Compounds Inducing Cellular Mitophagy
Ce CHEN1, 2, Kaikai JIN1, Yuanyuan WEI1, Qiongying HU1, 2, *
Affiliations
  • 1 The First People's Hospital of Wenling (Taizhou University Affiliated Wenling Hospital), School of Medicine, Taizhou University, Taizhou 318000, China
  • 2 Hebei Key Laboratory of Neuropharmacology, Department of Pharmacy,Hebei North University, Zhangjiakou 075000, China
出版时间: 2024-03-08
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摘要
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自噬是一种特殊的程序性细胞死亡方式,维持着生物体内的重要代谢和能量平衡,该过程涉及降解蛋白质、细胞器等成分。线粒体自噬是一种高度选择性自噬,可通过降解多余或受损线粒体实现自身代谢物及能量需要。线粒体自噬作为如今选择性自噬中研究较多的领域,在疾病的发生发展中占有重要地位。研究发现一些化合物可通过不同的线粒体信号通路诱导细胞发生自噬,从而影响疾病的进程。作者描述了线粒体自噬的诱导机制,并就诱导细胞线粒体自噬化合物进行探讨,以期为开发靶向线粒体的治疗药物提供参考。

选择性自噬  /  线粒体自噬  /  癌症  /  三萜  /  生物碱

Autophagy is a kind of programmed cell death that maintains metabolic and energetic homeostasis in organisms, which involves degradation of proteins, organelles, and other components. Mitophagy is a highly selective autophagy, which achieves its own metabolites and energy requirements by degrading excess or damaged mitochondria. Mitophagy plays an important role in the development of diseases, as one of selective autophagy most studied up to now. Some compounds have been found to induce mitophagy in cells through different mitochondrial signaling pathways, affecting the disease. In the current review, we summarized the mechanism of mitophagy induction and compounds that induce mitophagy are summarized, with the aim to provide a reference for the research and development of new drugs targeting mitochondria.

selective autophagy  /  mitophagy  /  cancer  /  triterpene  /  alkaloid
陈策, 金锴凯, 魏园园, 胡琼莹. 诱导细胞线粒体自噬化合物的研究进展. 中国药学杂志, 2024 , 59 (5) : 385 -391 .
Ce CHEN, Kaikai JIN, Yuanyuan WEI, Qiongying HU. Research Progress of Compounds Inducing Cellular Mitophagy[J]. Chinese Pharmaceutical Journal, 2024 , 59 (5) : 385 -391 .
正文
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自噬广泛存在于真核细胞内,是一种可通过消化细胞质内容物和处理细胞内废物来减轻细胞应激反应的高度保守的分解代谢过程。该过程涉及降解细胞内错误折叠或聚集的蛋白质、受损细胞器(如线粒体、内质网、溶酶体)等成分[1]。自噬的基本过程可分为5步[2],具体见图1。该过程涉及多种自噬相关基因(autophagy related gene,ATG)的精密调节。根据自噬降解细胞内成分是否具有选择性,可将自噬分为选择性自噬和非选择性自噬,线粒体自噬是一种高度选择性自噬。Lemasters等[3]证明线粒体自噬可以有效清除细胞内衰老和功能失调的线粒体,从而保护细胞免受线粒体代谢紊乱和促凋亡蛋白释放带来的伤害。随着对线粒体自噬的深入探索,人们发现线粒体自噬与癌症、神经退行性疾病、缺血、药物诱导的组织损伤等疾病有关[4]。此外,一些天然或人工化合物可通过多种线粒体作用途径促进细胞自噬,从而影响疾病的发生发展。因此,笔者就线粒体自噬的诱导机制及诱导细胞线粒体自噬化合物的研究进展作一综述。
1 选择性自噬的类型及诱导机制
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选择性自噬主要针对特定底物的降解,是清除受损和/或多余亚细胞细胞器的常见机制,包括线粒体介导的自噬(线粒体自噬)、内质网应激介导的自噬(内质网自噬)、溶酶体介导的自噬(溶酶体自噬)等[5]。
1.1 线粒体自噬
在上述针对亚细胞细胞器的不同自噬类型中,研究最多的属线粒体自噬。线粒体自噬是在2005年由Lemasters等[3]首次提出,是指在缺氧、活性氧(reactive oxygen species,ROS)、呼吸链抑制剂等多种刺激下,自噬相关关键蛋白通过识别衰老或受损线粒体上的特异性自噬受体,使隔离吞噬体靶向并完全包裹特定的单个去极化线粒体形成自噬体,自噬体发生酸化与溶酶体前体融合形成自噬溶酶体,从而特异性地降解被隔离的线粒体,进而维持细胞内环境的稳定。因此,线粒体自噬在线粒体质量控制中发挥着重要作用,是缓解细胞死亡和组织损伤的可能靶点。
线粒体自噬的诱导机制可分两类,一是泛素依赖性机制,主要指自噬蛋白LC3接头蛋白通过泛素依赖性机制识别泛素化的线粒体蛋白。其中同源性磷酸酶-张力蛋白诱导的激酶1(PTEN-induced putative kinase1,PINK1)/帕金蛋白(Parkin)介导的严重去极化线粒体降解途径已成为线粒体自噬过程的关键范式。正常线粒体通过线粒体外膜(outer mitochondrial membrane,OMM)转位酶(translocase of the OMM,TOM)和线粒体内膜(inner mitochondrial membrane,IMM)转位酶(translocase of the IMM,TIM)将PINK1转位至IMM,PINK1则会经过基质处理肽酶(matrix processing peptidase,MPP)和早老素相关菱形样蛋白酶(presenilin-associated rhomboid like,PARL)的处理被裂解[6]。在不同的致死条件下,受损的线粒体由于电子传递链的缺陷失去维持跨膜电位的能力或堆积异常折叠蛋白,不能将PINK1导入IMM,导致PINK1大量累积并稳定在OMM上,此时PINK1的自身磷酸化修饰能够识别并磷酸化Parkin泛素样(ubiquitin-like,Ubl)结构域中的Ser65位点[7],使得Parkin RBR E3泛素蛋白连接酶(parkin RBR E3 ubiquitin protein ligase,PRKN)从细胞质募集和活化至OMM[6]。PRKN还会进一步放大PINK1的上游信号,该信号将磷酸泛素链连接到OMM蛋白[包括电压依赖阴离子通道(voltage dependent anion channels,VDAC)、ras同源家族成员T1(ras homolog family member T1,RHOT1/MIRO1)、线粒体融合蛋白1(mitofusin 1,MFN1)和MFN2],形成底物-多聚泛素链(poly-Ub,PUb)。同时,LC3接头蛋白(SQSTM1/p62 、OPTN、CALCOCO2/NDP52、TAX1BP1 和NBR1)识别PUb,并通过LC3结合域(LC3 interacting region, LIR)与LC3B相互作用,在受损线粒体上形成自噬体。这些受体(尤其是OPTN)可以被TANK结合激酶1(TANK-binding kinase 1,TBK1)磷酸化,从而增加与PUb结合的亲和力。而在不依赖Parkin的情况下,OPTN和CALCOCO2/NDP52可以被PINK1直接招募,随后通过激活自噬起始因子unc-51样激酶1(unc-51 like kinase 1, ULK1)、DFCP1和 WIPI1启动自噬体生物发生。此外,SIAH1、MUL1和ARIH1等作为E3泛素连接酶,可参与泛素型线粒体自噬过程[5]。见图2。
二是泛素非依赖型机制,此时的线粒体自噬主要由受体介导,见图3。其中线粒体膜上未泛素化的蛋白可被LC3接头蛋白识别并结合,如胆碱脱氢酶(choline dehydrogenase,CHDH)与SQSTM1/p62相互作用以招募LC3;TBC1结构域家族成员15(TBC1 domain family member 15,TBC1D15)和TBC1D17通过其受体Fis1靶向OMM来调控自噬体的形成[7]。而OMM上的LC3受体(如BNIP3L/NIX、BNIP3、FUNDC1、FKBP8、BCL2L13、DISC1、NLRX1)通过典型或非典型LIR基序[5],能够直接与LC3和/或GABARAP相互作用。其中特别的是,AMBRA1能够以Parkin依赖和不依赖的方式启动线粒体自噬。与OMM定位的线粒体自噬受体不同,定位于IMM的PHB2受体的调节主要依赖Parkin。此外,心磷脂(cardiolipin,CL)作为IMM特征性磷脂,在线粒体应激或转位时,可以外化作为线粒体自噬受体。有研究指出,在基础水平或慢性应激条件下,受体介导的线粒体自噬高速率运作,而PINK1/Parkin通路可补偿由急性化学损伤引起的线粒体功能障碍[4]。
1.2 内质网自噬
除了线粒体自噬,人们对内质网应激介导的自噬研究也较多。内质网应激是指当内质网稳态遭到破坏时(如错误折叠的蛋白质聚集、Ca2+耗竭等),通过相应的信号通路引发的细胞内一系列反应[8]。内质网应激介导的自噬机制主要包括未折叠蛋白质反应(unfolded protein response,UPR)依赖性自噬机制,涉及内质网到核的信号传导1(endoplasmic reticulum to nucleus signaling 1,ERN1/IRE1α)、真核翻译起始因子2α激酶3(eukaryotic translation initiation factor 2 alpha kinase 3,EIF2AK3/PERK)和激活转录因子6(activating transcription factor 6,ATF6)介导的信号通路[5],以及Ca2+依赖的AMPK-mTOR信号通路途径等[9]。有趣的是,Rubio等[10]研究发现当内质网发生光损失时,细胞早期以发生内质网自噬为主,但随着内质网自噬的增加,会进一步激活线粒体自噬,导致后期以发生线粒体自噬为主,说明内质网自噬会诱导线粒体自噬的发生。因此,在本质上,最后是以线粒体自噬为主要细胞死亡方式。
1.3 溶酶体自噬
此外,溶酶体作为自噬的必需场所,及时清除受损溶酶体对细胞存活至关重要。溶酶体自噬主要受泛素依赖性[如半乳糖凝集素-3(galectin-3,Gal3)-三重基序家族蛋白TRIM16-ULK1-自噬接头蛋白-LC3,E2泛素结合酶UBE2QL1-自噬接头蛋白-LC3等]和泛素非依赖性[半乳糖凝集-8(galectin-8,Gal8)-自噬受体NDP52-LC3]等途径调控[11]。
总的来说,这3种细胞器介导自噬的途径有着较大的区别,但本质上都是激活细胞器膜上相应蛋白继而被自噬相关受体识别诱导自噬。独特的是如上述所说内质网自噬可促进线粒体自噬,这使得靶向线粒体治疗成为可能。表1是这3种细胞器介导自噬的差异。
2 诱导线粒体自噬的化合物
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随着对线粒体自噬的深入研究,越来越多的证据表明,线粒体自噬的异常与心力衰竭,神经退行性病变,癌症和衰老等疾病有关。因此,一些被证明可调节线粒体自噬的天然或人工合成的化合物可能具有潜在治疗前景。具体总结见表2。以下重点阐述了几个研究较为深入的化合物及其调控线粒体自噬的作用机制。
2.1 真菌提取衍生物
真菌聚酮(cytosporone B,Csn-B)来源于内生真菌小穴壳菌,研究表明其具有良好的抗肿瘤药理活性[24]。研究报道[12]了一种Csn-B衍生物1-(3,4,5-三羟基苯基)壬-1-酮[1-(3,4,5- trihydroxyphenyl)nonan-1-one,THPN],这是一种孤儿核受体Nur77的新型靶向化合物。研究发现在THPN的刺激下,Nur77可通过OMM蛋白NIX介导的线粒体信号途径诱导黑色素瘤细胞发生自噬性死亡。THPN能与Nur77上特定的C端配体结合域相结合,从而增强Nur77与NIX相互作用,并在NIX的辅助下Nur77可从细胞质转运到OMM,而后在OMM通道Tom复合体的引导下进入IMM,Nur77的转录激活域继而与IMM上的腺嘌呤核苷酸转位酶1(adenin nukleotid translokáza,ANT1)结合。ANT1是膜孔通道复合体(mitochondrial permeability transition pore complex, mPTPC)上的关键蛋白,它的激活能促进mPTPC孔道的开放,通过ANT1-VDAC1复合物使得线粒体的膜电位下降和ATP能量异常,促进自噬的发生,最终导致线粒体的过度清除以及黑色素瘤细胞走向不可逆的自噬性死亡[12]。
2.2 植物提取物及其衍生物
2.2.1 雷公藤红素
雷公藤红素(celastrol)来源于卫矛科雷公藤属植物,是雷公藤中活性较强的有效成分,是一种典型的三萜类化合物,研究表明[25]雷公藤具有较强的抗炎、抗肿瘤作用。研究[13]发现,暴露于炎症因子TNFα的肝癌细胞在雷公藤红素的作用下可发生Nur77依赖性线粒体介导的自噬,从而缓解炎症。实验中雷公藤红素可与Nur77相互结合并促进Nur77从细胞核易位至受损线粒体上,接着Nur77与肿瘤坏死因子受体相关因子2 (tumor necrosis factor receptor associated factor 2,TRAF2)相互作用引起Nur77泛素化,被泛素化修饰的Nur77会停留在线粒体上并进一步与泛素接合蛋白p62/SQSTM1互作用,同时促进自噬体的形成,最终导致肝癌细胞发生自噬[13]。
2.2.2 环维黄杨星D(cyclovirobuxine D,CVB-D)
CVB-D是中药黄杨中的一种天然的生物碱成分,主要用于治疗心脑血管疾病,近年来,有研究[14]表明CVB-D可能具有抗肿瘤作用。该研究发现CVB-D可诱导肺癌细胞发生线粒体自噬。CVB-D可通过下调核转录因子p65促进OMM蛋白BNIP3的表达,BNIP3继而与LC3相互作用,形成线粒体BNIP3-LC3-自噬体复合体,并介导线粒体自噬激活,表明CVB-D可通过p65/BNIP3/LC3途径诱导线粒体自噬[14]。
2.2.3 银杏酸(ginkgolic acid,GA)
GA是从银杏叶、果仁和种皮中提取的天然成分,具有抗肿瘤、促凋亡、促自噬等多种生物活性[26]。研究[15]发现,GA可诱导宫颈癌细胞HeLa细胞中的线粒体破碎,减少线粒体DNA拷贝数和线粒体蛋白水平,并损害线粒体腺苷5'-三磷酸的产生和氧气消耗。此外,通过敲除自噬蛋白Atg7或使用自噬抑制剂消除自噬可以恢复GA诱导的线粒体质量减少。而OMM蛋白FUNDC1基因敲低后恢复了GA诱导的线粒体质量减少和线粒体膜电位损失的变化。说明GA通过减少线粒体生物发生和促进FUNDC1依赖性线粒体自噬来损害线粒体功能[15]。
2.2.4 人参皂苷Rh2
人参皂苷Rh2是人参中提取的一种固醇类化合物,一些研究表明人参皂苷Rh2可通过诱导细胞周期停滞和线粒体依赖性细胞凋亡来增强抗癌特性。研究[16]发现,由多柔比星诱导的分泌性衰老上皮细胞可促进乳腺癌细胞MCF-7的增殖,同时降低正常上皮细胞的存活率,而人参皂苷Rh2可显著缓解这种情况,可通过增加OMM蛋白PINK1和Parkin的表达以及降低过氧化物酶体增殖受体γ辅激活因子(peroxisome proliferators activated receptor gamma coactivator-alpha,PGC-1α)的水平显著促进线粒体自噬。这表明人参皂苷Rh2是一种潜在的治疗衰老相关疾病的候选药物[16]。
2.2.5 白藜芦醇苷(polydatin,PD)
PD是从中药虎杖中分离出来的单晶药物,广泛用于治疗烧伤、器官功能障碍[27]。研究[17]发现,PD可以促进Parkin易位至线粒体,并促进由脂多糖(lipopolysaccharide,LPS)处理的人正常肺上皮细胞BEAS-2B细胞的线粒体自噬。然而PD诱导的线粒体自噬在Parkin基因敲低的小鼠和细胞中被抑制,表明PD激活了Parkin依赖性的线粒体自噬。
2.2.6 二苯乙烯苷(tetrahydroxystilbene glucoside,TSG)
TSG是何首乌的主要活性成分之一,具有保护肝脏、降低血液胆固醇、抗氧化和抗动脉粥样硬化的作用,文献[28]也报道TSG在脑损伤修复中具有保护作用。研究[18]发现TSG可以逆转LPS或β-淀粉样纤维肽(β-amyloid fibrillary peptide,Aβ)对小鼠原代小胶质细胞自噬通量的抑制作用,可通过AMPK/PINK1/Parkin依赖性通路增强线粒体自噬。该研究结果发现TSG可以显著促进AMPK的磷酸化,并通过STRING富集分析确定了AMPK/PINK1/PARKIN信号通路。该实验进一步证明了缺乏PINK1会抑制小胶质细胞的自噬,尤其是线粒体自噬。此外,通过敲低PINK1或Parkin基因可以消除TSG的保护作用[18]。总之TSG可通过AMPK相关的PINK1/Parkin信号通路介导线粒体自噬来减轻炎症损伤。
2.2.7 Nujiangexanthone A(NJXA)
NJXA是从怒江藤黄叶片中分离得到的一种活性成分,具有抗肿瘤作用。研究[19]发现NJXA可通过促进线粒体自噬诱导HeLa细胞死亡。该研究结果发现NJXA可促进线粒体发生去极化,促进PINK1在OMM的稳定表达,使得Parkin发生降解,且OMM蛋白Tom20和内膜蛋白Tim23以及融合蛋白MFN1和MFN2在NJXA处理后也发生了明显降解,表明NJXA诱导HeLa细胞的自噬可能是Parkin依赖性的方式,此外NJXA也显著增强了Parkin与p62和LC3的共定位[19]。说明NJXA可通过PINK1/Parkin/p62信号通路诱导线粒体自噬。
2.2.8 青蒿琥酯(artesunate,ART)
ART来源于青蒿,是青蒿素的一种水溶性衍生物,被广泛用于治疗疟疾,研究表明其也有显著的抗癌特性[20]。Zhang等[20]研究发现,在宫颈癌细胞HeLa细胞中ART主要定位于线粒体且可以促使自噬发生和线粒体蛋白的减少,当自噬受到抑制时,线粒体蛋白的减少可以被逆转,说明线粒体蛋白的降解是通过自噬实现的。该研究进一步发现ART可以促进PINK1的稳定表达,继而促使Parkin、p62、LC3招募至线粒体,并使得线粒体自噬达到顶峰。然而当PINK1被敲低时,ART诱导的线粒体自噬被显著抑制,说明ART通过PINK1依赖性通路诱导线粒体自噬。此外,抑制PINK1可显著增加ART诱导的线粒体去极化和更多的细胞凋亡,表明线粒体自噬保护了ART诱导的细胞死亡[20]。总之,ART可通过PINK1途径诱导细胞发生保护性线粒体自噬。
2.2.9 尿石素A(urolithin A,UA)
UA是在人体肠道菌群作用下从天然多酚化合物鞣花单宁(ellagitannins,ETs)中产生的一种次生代谢产物,具有抗衰老,抗炎,抗氧化以及调节线粒体自噬等广泛的生物活性[29]。有研究[21]发现,病变关节的软骨细胞可通过诱导线粒体自噬积累功能失调的线粒体,因此,为进一步探寻UA在骨关节炎(osteoarthritis,OA)临床前模型中挽救线粒体自噬的药理学方法,Davide等[21]基于体外和体内模型,发现低剂量的UA在人软骨细胞中能够通过介导的pUb,显著诱导编码Parkin和p62蛋白的自噬/自噬标志物PARK2和SQSTM1,以及MAP1LC3B的水平的增加。并且与原OA小鼠膝关节相比,UA治疗后的关节软骨中TOM20蛋白和关节pUb水平显著提高。这表明UA在OA中可通过调节PINK1/Parkin/泛素依赖的线粒体自噬通路,诱导线粒体自噬[21]。
2.3 神经递质衍生物
6-羟基多巴胺(6-OHDA)是一种儿茶酚胺的羟基化衍生物,是一类高效的神经毒剂,能有效导致多巴胺神经元变性[30]。研究[22]发现,6-OHDA可促进嗜铬细胞瘤细胞PC12中孤儿核受体Nur77的表达并使其易位至受损线粒体上,继而激活PINK1/Parkin信号通路,并最终导致细胞发生自噬,加重细胞的损伤。
2.4 其他
硝唑尼特(nitazoxanide,NTZ)是一种抗原虫药物,最初用于治疗肠道寄生虫引起的感染性腹泻,也有抗蠕虫、抗肿瘤等特性[31]。研究[23]发现,NTZ可通过PINK1生成的磷酸化-泛素化(pS65-Ub)和自噬受体介导的通路诱导线粒体损伤和线粒体自噬。该研究结果证明,NTZ可显著促进PINK1的表达,并进一步招募自噬受体OPTN和NDP52聚集于线粒体诱导线粒体自噬,从而抑制膀胱癌的发展。
3 总结
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细胞通过线粒体自噬清除多余或受损的线粒体,从而维持细胞内环境稳态。线粒体在多种疾病中起着重要作用,通过诱导线粒体自噬促进细胞死亡从而影响疾病的发展进程,如上述提及的癌症、神经退行性疾病等。笔者综述了线粒体自噬的诱导机制,并详细阐述了可诱导细胞线粒体自噬的化合物,涵盖了真菌、植物等领域,体现了调节线粒体自噬化合物的多样性。这使得靶向线粒体成为一个潜在的治疗策略。
线粒体自噬作为如今生物医学研究的热点,目前还存在一些关键问题需要阐明,如:①自噬体的双层膜结构是否可能来源于受损的线粒体,若来源于线粒体,其具体机制是怎样的;②一些线粒体具体机制还有待完善,如AMPK信号通路中的哪些关键分子诱导PINK1/Parkin,进而启动线粒体自噬;③除线粒体外,高尔基体作为细胞分泌物最后加工和包装的场所,也是细胞内必不可少的细胞器,虽已有研究证明其与自噬存在一定联系[32],但涉及的具体分子机制仍未被发现。因此,是否可以通过同步调节不同类型细胞器特异性自噬的活性,指导线粒体自噬发展,仍有待进一步研究; ④除了目前已知的线粒体自噬受体,是否有其他的线粒体自噬受体存在于特定的组织或细胞中。而现阶段线粒体自噬的研究大多局限于细胞、动物等基础实验层面,临床研究资料有限。基于上述问题,希望未来能够:深入研究线粒体自噬的具体过程与机制,探寻不同组织或细胞特殊的线粒体自噬靶点和通路,并进一步探究线粒体自噬与其他选择性自噬内在的相关性。总之,深入探索线粒体自噬的调控机制有助于人们为开发靶向线粒体的治疗药物奠定理论基础。
基金
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  • 浙江省基础公益研究计划项目资助(LGF21H280002)
文献
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参考文献 引证文献
排序方式：
[1]
CHEN L, FAN F, WU L, et al. The nuclear receptor 4A family members: mediators in human disease and autophagy[J]. Cell Mol Biol Lett, 2020, 25(1):48. DOI 10.1186/s11658-020-00241-w.
[2]
CADWELL K, DEBNATH J. Beyond self-eating: the control of nonautophagic functions and signaling pathways by autophagy-related proteins[J]. J Cell Biol, 2018, 217(3): 813-822.
[3]
KIM I, RODRIGUEZ-ENRIQUEZ S, LEMASTERS J J. Selective degradation of mitochondria by mitophagy[J]. Arch Biochem Biophy, 2007, 462(2): 245-253.
[4]
CHOUBEY V, ZEB A, KAASIK A. Molecular mechanisms and regulation of mammalian mitophagy[J]. Cells, 2021, 11(1):38. DOI: 10.3390/cells11010038.
[5]
YAO R Q, REN C, XIA Z F, et al. Organelle-specific autophagy in inflammatory diseases: a potential therapeutic target underlying the quality control of multiple organelles[J]. Autophagy, 2021, 17(2): 385-401.
[6]
NGUYEN T N, PADMAN B S, LAZAROU M. Deciphering the molecular signals of PINK1/Parkin mitophagy[J]. Trends Cell Biol, 2016, 26(10): 733-744.
[7]
ONISHI M, YAMANO K, SATO M, et al. Molecular mechanisms and physiological functions of mitophagy[J]. The EMBO J, 2021, 40(3): e104705. DOI: 10.15252/embj.2020104705.
[8]
LIU C L, HE K L, WANG L L. Research progress of cell protection strategy based on endoplasmic reticulum stress pathway[J]. Chin Pharmacol Bull (中国药理学通报), 2011, 27(4): 455-458.
[9]
HØYER-HANSEN M, BASTHOLM L, SZYNIAROWSKI P, et al. Control of macroautophagy by calcium, calmodulin-dependent kinase kinase-beta, and Bcl-2[J]. Mol Cell, 2007, 25(2): 193-205.
[10]
RUBIO N, COUPIENNE I, DI VALENTIN E, et al. Spatiotemporal autophagic degradation of oxidatively damaged organelles after photodynamic stress is amplified by mitochondrial reactive oxygen species[J]. Autophagy, 2012, 8(9): 1312-1324.
[11]
PAPADOPOULOS C, KRAVIC B, MEYER H. Repair or lysophagy: dealing with damaged lysosomes[J]. J Mol Biol, 2020, 432(1): 231-239.
[12]
WANG W J, WANG Y, CHEN H Z, et al. Orphan nuclear receptor TR3 acts in autophagic cell death via mitochondrial signaling pathway[J]. Nat Chem Biol, 2014, 10(2): 133-140.
[13]
HU M, LUO Q, ALITONGBIEKE G, et al. Celastrol-Induced Nur77 Interaction with TRAF2 Alleviates Inflammation by Promoting Mitochondrial Ubiquitination and Autophagy[J]. Mol Cell, 2017, 66(1): 141-53.e6.
[14]
ZENG C, ZOU T, QU J, et al. Cyclovirobuxine D induced-mitophagy through the p65/BNIP3/LC3 axis potentiates its apoptosis-inducing effects in lung cancer cells[J]. Int J Mol Sci, 2021, 22(11):5820. DOI: 10.3390/ijms22115820.
[15]
WANG W, WANG M, RUAN Y, et al. Ginkgolic acids impair mitochondrial function by decreasing mitochondrial biogenesis and promoting FUNDC1-dependent mitophagy[J]. J Agric Food Chem, 2019, 67(36): 10097-10106.
[16]
HOU J, YUN Y, XUE J, et al. Doxorubicin-induced normal breast epithelial cellular aging and its related breast cancer growth through mitochondrial autophagy and oxidative stress mitigated by ginsenoside Rh2[J]. Phytother Res, 2020, 34(7): 1659-1669.
[17]
LI T, LIU Y, XU W, et al. Polydatin mediates Parkin-dependent mitophagy and protects against mitochondria-dependent apoptosis in acute respiratory distress syndrome[J]. Lab Invest, 2019, 99(6): 819-829.
[18]
GAO Y, LI J, LI J, et al. Tetrahydroxy stilbene glycoside alleviated inflammatory damage by mitophagy via AMPK related PINK1/Parkin signaling pathway[J]. Biochem Pharmacol, 2020, 177: 113997. DOI: 10.1016/j.bcp.2020.113997.
[19]
FENG J, MANSOURIPOUR A, XI Z, et al. Nujiangexanthone A inhibits cervical cancer cell proliferation by promoting mitophagy[J]. Molecules (Basel, Switzerland), 2021, 26(10):2858. DOI: 10.3390/molecules26102858.
[20]
ZHANG J, SUN X, WANG L, et al. Artesunate-induced mitophagy alters cellular redox status[J]. Redox Biol, 2018, 19: 263-273.
[21]
D'AMICO D, OLMER M, FOUASSIER A M, et al. Urolithin A improves mitochondrial health, reduces cartilage degeneration, and alleviates pain in osteoarthritis[J]. Aging Cell, 2022, 21(8): e13662. DOI: 10.1111/acel.13662.
[22]
GAO H, CHEN Z, FU Y, et al. Nur77 exacerbates PC12 cellular injury in vitro by aggravating mitochondrial impairment and endoplasmic reticulum stress[J]. Sci Rep, 2016, 6: 34403. DOI: 10.1038/srep34403.
[23]
SUN H, OU T, HU J, et al. Nitazoxanide impairs mitophagy flux through ROS-mediated mitophagy initiation and lysosomal dysfunction in bladder cancer[J]. Biochem Pharmacol, 2021, 190: 114588. DOI: 10.1016/j.bcp.2021.114588.
[24]
ZHAN Y, DU X, CHEN H, et al. Cytosporone B is an agonist for nuclear orphan receptor Nur77[J]. Nat Chem Biol, 2008, 4(9): 548-556.
[25]
LI N, ZHANG T D, WANG Y F, et al. Autophagy of human HeLa cells induced by tripterine in vitro and in vivo and its molecular mechanism[J]. Chin Pharm J(中国药学杂志), 2018, 53(7): 513-517.
[26]
QI Q M, XUE Y C, LV J, et al. Ginkgolic acids induce HepG2 cell death via a combination of apoptosis, autophagy and the mitochondrial pathway[J]. Oncol Lett, 2018, 15(5): 6400-6408.
[27]
LI T, CAI S, ZENG Z, et al. Protective effect of polydatin against burn-induced lung injury in rats[J]. Respir Care, 2014, 59(9): 1412-1421.
[28]
LI F, ZHANG T, HE Y, et al. Inflammation inhibition and gut microbiota regulation by TSG to combat atherosclerosis in ApoE(-/-) mice[J]. J Ethnopharmacol, 2020, 247: 112232. DOI: 10.1016/j.jep.2019.112232.
[29]
D'AMICO D, ANDREUX P A, VALDÉS P, et al. Impact of the natural compound urolithin A on health, disease, and aging [J]. Trends Mol Med, 2021, 27(7): 687-699.
[30]
YUAN X, YE Y, XUE Z. 6-OHDA-induced Parkinson's disease mice showed a senescence phenotype characterized by up-regulation of p16-(Ink4a) and astrocyte senescence[J]. J Shanghai Jiao Tong Univ(Med Ed)(上海交通大学学报医学版), 2021, 41(7): 876-883.
[31]
ROSSIGNOL J F. Nitazoxanide: a first-in-class broad-spectrum antiviral agent[J]. Antiviral Res, 2014, 110: 94-103.
[32]
SHOJI-KAWATA S, SUMPTER R, LEVENO M, et al. Identification of a candidate therapeutic autophagy-inducing peptide[J]. Nature, 2013, 494(7436): 201-206.
2024年第59卷第5期
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  • 接收时间：2023-10-14
  • 首发时间：2026-04-08
  • 出版时间：2024-03-08
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  • 收稿日期：2023-10-14
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浙江省基础公益研究计划项目资助(LGF21H280002)
作者信息
    1 温岭市第一人民医院(台州学院附属温岭医院), 台州学院医学院, 浙江 台州 318000
    2 河北北方学院药学院, 河北省神经药理学重点实验室, 河北 张家口 075000

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*胡琼莹,女,博士,教授 研究方向:抗肿瘤、抗感染药物的发现及作用机制研究 Tel:(0576)88665198
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Number of
species		 占总种数比例
Percentage of
total species (%)		 属
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Number of
species		 占总种数比例
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鹅膏菌科Amanitaceae 2 11 5.26 鹅膏菌属 Amanita 10 4.78
小菇科 Mycenaceae 2 12 5.74 丝盖伞属 Inocybe 5 2.39
多孔菌科 Polyporaceae 8 14 6.70 蜡蘑属 Laccaria 5 2.39
红菇科 Russulaceae 3 23 11.00 小皮伞属 Marasmius 6 2.87
小菇属 Mycena 11 5.26
光柄菇属 Pluteus 5 2.39
红菇属 Russula 17 8.13
栓菌属 Trametes 5 2.39
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