[1]吴安然,张文怡,张国伟,等.PINK1/Parkin介导的线粒体自噬在眼科疾病中作用的研究进展[J].眼科新进展,2023,43(3):238-243.[doi:10.13389/j.cnki.rao.2023.0049]
　WU Anran,ZHANG Wenyi,ZHANG Guowei,et al.Research progress on the role of PTEN-induced novel kinase 1/Parkin-mediated mitophagy in eye diseases[J].Recent Advances in Ophthalmology,2023,43(3):238-243.[doi:10.13389/j.cnki.rao.2023.0049]
点击复制

PINK1/Parkin介导的线粒体自噬在眼科疾病中作用的研究进展/HTML
分享到：

《眼科新进展》[ISSN:1003-5141/CN:41-1105/R]

卷:
43卷
期数:
2023年3期
页码:
238-243
栏目:
文献综述
出版日期:
2023-03-05

文章信息/Info

Title:
Research progress on the role of PTEN-induced novel kinase 1/Parkin-mediated mitophagy in eye diseases
作者:
吴安然; 张文怡; 张国伟; 管怀进
226001　江苏省南通市，南通大学附属医院眼科，南通大学医学院（吴安然，张文怡）；226001　江苏省南通市，南通大学附属医院眼科（张国伟，管怀进）
Author(s):
WU Anran1; ZHANG Wenyi1; ZHANG Guowei2; GUAN Huaijin2
1.Eye Institute,Affiliated Hospital of Nantong University,Medical School of Nantong University,Nantong 226001,Jiangsu Province,China
2.Eye Institute,Affiliated Hospital of Nantong University,Nantong 226001,Jiangsu Province,China
关键词:
眼科疾病; 线粒体; 线粒体自噬; PINK1/Parkin信号通路
Keywords:
eye diseases;  mitochondria;  mitophagy;  PTEN-induced novel kinase 1/Parkin signaling pathway
分类号:
R77
DOI:
10.13389/j.cnki.rao.2023.0049
文献标志码:
A
摘要:
线粒体自噬作为一种选择性自噬过程，通过清除受损和多余线粒体来维持细胞正常生理功能。线粒体自噬与多种眼科疾病的发生发展有密切联系，而PINK1/Parkin信号通路作为线粒体自噬的主要通路之一，在白内障、青光眼、年龄相关性黄斑变性等多种眼科疾病中发挥了重要作用，靶向该通路的治疗手段也为多种眼科疾病的治疗提供了新思路。本文将对PINK1/Parkin介导的线粒体自噬通路在眼科疾病中的相关作用及机制进行综述，以期深入了解线粒体自噬在眼科相关疾病中的影响与价值。
Abstract:
Mitophagy, as a selective autophagy process, maintains the normal physiological function of cells by removing damaged and excess mitochondria. Mitophagy is closely related to the occurrence and development of various eye diseases. The PTEN-induced novel kinase 1 (PINK1)/Parkin signaling pathway, as one of the main pathways of mitophagy, plays an essential role in various eye diseases such as cataract, glaucoma, and age-related macular degeneration. The therapeutic methods targeting this pathway also provide a new idea for the treatment of many eye diseases. This article will review the role and mechanism of PINK1/Parkin-mediated mitophagy pathway in eye diseases, in order to further understand the influence and value of mitophagy in eye diseases.

参考文献/References:

［1］　SPRINGER M Z,MACLEOD K F.In brief:mitophagy:mechanisms and role in human disease［J］．J Pathol,2016,240(3):253-255.
［2］　LEMASTERS J J.Selective mitochondrial autophagy,or mitophagy,as a targeted defense against oxidative stress,mitochondrial dysfunction,and aging［J］．Rejuvenation Res,2005,8(1):3-5.
［3］　KIM I,RODRIGUEZ-ENRIQUEZ S,LEMASTERS J J.Selective degradation of mitochondria by mitophagy［J］．Arch Biochem Biophys,2007,462(2):245-253.
［4］　DOBLADO L,LUECK C,REY C,SAMHAN-ARIAS A K,PRIETO I,STACCHIOTTI A,et al.Mitophagy in human diseases［J］．Int J Mol Sci,2021,22(8):3903.
［5］　LEMASTERS J J.Variants of mitochondrial autophagy:types 1 and 2 mitophagy and micromitophagy(type 3)［J］．Redox Biol,2014,2:749-754.
［6］　ASHRAFI G,SCHWARZ T L.The pathways of mitophagy for quality control and clearance of mitochondria［J］．Cell Death Differ,2013,20(1):31-42.
［7］　GREENE A W,GRENIER K,AGUILETA M A,MUISE S,FARAZIFARD R,HAQUE M E,et al.Mitochondrial processing peptidase regulates PINK1 processing,import and parkin recruitment［J］．EMBO Rep,2012,13(4):378-385.
［8］　WEIL R,LAPLANTINE E,CURIC S,GENIN P.Role of optineurin in the mitochondrial dysfunction:potential implications in neurodegenerative diseases and cancer［J］．Front Immunol,2018,9:1243.
［9］　URBAN S,FREEMAN M.Substrate specificity of rhomboid intramembrane proteases is governed by helix-breaking residues in the substrate transmembrane domain［J］．Mol Cell,2003,11(6):1425-1434.
［10］　PICKRELL A M,YOULE R J.The roles of PINK1,parkin,and mitochondrial fidelity in Parkinson’s disease［J］．Neuron,2015,85(2):257-273.
［11］　AGARWAL S,MUQIT M M K.PTEN-induced kinase 1(PINK1) and parkin:unlocking a mitochondrial quality control pathway linked to Parkinson’s disease［J］．Curr Opin Neurobiol,2022,72:111-119.
［12］　WAUER T,SIMICEK M,SCHUBERT A,KOMANDER D.Mechanism of phospho-ubiquitin-induced parkin activation［J］．Nature,2015,524(7565):370-374.
［13］　SUKHORUKOV V,VORONKOV D,BARANICH T,MUDZHIRI N,MAGNAEVA A,ILLARIOSHKIN S.Impaired mitophagy in neurons and glial cells during aging and age-related disorders［J］．Int J Mol Sci,2021,22(19):10251.
［14］　POOLE L P,MACLEOD K F.Mitophagy in tumorigenesis and metastasis［J］．Cell Mol Life Sci,2021,78(8):3817-3851.
［15］　SPRINGER M Z,POOLE L P,DRAKE L E,BOCK-HUGHES A,BOLAND M L,SMITH A G,et al.BNIP3-dependent mitophagy promotes cytosolic localization of LC3B and metabolic homeostasis in the liver［J］．Autophagy,2021,17(11):3530-3546.
［16］　MACVICAR T.Mitophagy［J］．Essays Biochem,2013,55:93-104.
［17］　HU J,KAN T,HU X.Sirt3 regulates mitophagy level to promote diabetic corneal epithelial wound healing［J］．Exp Eye Res,2019,181:223-231.
［18］　MIYAI T,VASANTH S,MELANGATH G,DESHPANDE N,KUMAR V,BENISCHKE A S,et al.Activation of PINK1-parkin-mediated mitophagy degrades mitochondrial quality control proteins in Fuchs endothelial corneal dystrophy［J］．Am J Pathol,2019,189(10):2061-2076.
［19］　BASSNETT S.Mitochondrial dynamics in differentiating fiber cells of the mammalian lens［J］．Curr Eye Res,1992,11(12):1227-1232.
［20］　BRENNAN L A,KANTOROW M.Mitochondrial function and redox control in the aging eye:role of MsrA and other repair systems in cataract and macular degenerations［J］．Exp Eye Res,2009,88(2):195-203.
［21］　PENDERGRASS W,PENN P,POSSIN D,WOLF N.Accumulation of DNA,nuclear and mitochondrial debris,and ROS at sites of age-related cortical cataract in mice［J］．Invest Ophthalmol Vis Sci,2005,46(12):4661-4670.
［22］　PENDERGRASS W,ZITNIK G,URFER S R,WOLF N.Age-related retention of fiber cell nuclei and nuclear fragments in the lens cortices of multiple species［J］．Mol Vis,2011,17:2672-2684.
［23］　COSTELLO M J,JOHNSEN S,GILLILAND K O,FREEL C D,FOWLER W C.Predicted light scattering from particles observed in human age-related nuclear cataracts using mie scattering theory［J］．Invest Ophthalmol Vis Sci,2007,48(1):303-312.
［24］　COSTELLO M J,BRENNAN L A,BASU S,CHAUSS D,MOHAMED A,GILLILAND K O,et al.Autophagy and mitophagy participate in ocular lens organelle degradation［J］．Exp Eye Res,2013,116:141-150.
［25］　ZHAO J,XU X,ELLWEIN L B,GUAN H,HE M,LIU P,et al.Causes of visual impairment and blindness in the 2006 and 2014 nine-province surveys in rural China［J］．Am J Ophthalmol,2019,197:80-87.
［26］　MARCHETTI M A,LEE W,COWELL T L,WELLS T M,WEISSBACH H,KANTOROW M.Silencing of the methionine sulfoxide reductase A gene results in loss of mitochondrial membrane potential and increased ROS production in human lens cells［J］．Exp Eye Res,2006,83(5):1281-1286.
［27］　BRENNAN L A,LEE W,COWELL T,GIBLIN F,KANTOROW M.Deletion of mouse MsrA results in HBO-induced cataract:MsrA repairs mitochondrial cytochrome C［J］．Mol Vis,2009,15:985-999.
［28］　BROOKS M M,NEELAM S,FUDALA R,GRYCZYNSKI I,CAMMARATA P R.Lenticular mitoprotection.Part A:monitoring mitochondrial depolarization with JC-1 and artifactual fluorescence by the glycogen synthase kinase-3β inhibitor,SB216763［J］．Mol Vis,2013,19:1406-1412.
［29］　BRENNAN L,KHOURY J,KANTOROW M.Parkin elimination of mitochondria is important for maintenance of lens epithelial cell ROS levels and survival upon oxidative stress exposure［J］．Biochim Biophys Acta Mol Basis Dis,2017,1863(1):21-32.
［30］　GUPTA N,YUCEL Y H.Glaucoma as a neurodegenerative disease［J］．Curr Opin Ophthalmol,2007,18(2):110-114.
［31］　DAI Y,WEINREB R N,KIM K Y,NGUYEN D,PARK S,SUN X,et al.Inducible nitric oxide synthase-mediated alteration of mitochondrial Opa1 expression in ocular hypertensive rats［J］．Invest Ophthalmol Vis Sci,2011,52(5):2468-2476.
［32］　JAHANI-ASL A,PILON-LAROSE K,XU W,MACLAURIN J G,PARK D S,MCBRIDE H M,et al.The mitochondrial inner membrane GTPase,optic atrophy 1 (Opa1),restores mitochondrial morphology and promotes neuronal survival following excitotoxicity［J］．J Biol Chem,2011,286(6):4772-4782.
［33］　NGUYEN D,ALAVI M V,KIM K Y,KANG T,SCOTT R T,NOH Y H,et al.A new vicious cycle involving glutamate excitotoxicity,oxidative stress and mitochondrial dynamics［J］．Cell Death Dis,2011,2(12):e240.
［34］　GROHM J,KIM S W,MAMRAK U,TOBABEN S,CASSIDY-STONE A,NUNNARI J,et al.Inhibition of Drp1 provides neuroprotection in vitro and in vivo［J］．Cell Death Differ,2012,19(9):1446-1458.
［35］　HU X,DAI Y,SUN X.Parkin overexpression protects retinal ganglion cells against glutamate excitotoxicity［J］．Mol Vis,2017,23:447-456.
［36］　DAI Y,HU X,SUN X.Overexpression of parkin protects retinal ganglion cells in experimental glaucoma［J］．Cell Death Dis,2018,9(2):88.
［37］　YAN Y Q,FANG Y,ZHENG R,PU J L,ZHANG B R.NLRP3 inflammasomes in Parkinson’s disease and their regulation by parkin［J］．Neuroscience,2020,446:323-334.
［38］　WU X,DOU Y N,FEI Z,FEI F.Parkin prevents glutamate excitotoxicity through inhibiting NLRP3 inflammasome in retinal ganglion cells［J］．Neuroscience,2021,478:1-10.
［39］　JACOMIN A C,TAILLEBOURG E,FAUVARQUE M O.Deubiquitinating enzymes related to autophagy:new therapeutic opportunities?［J］．Cells,2018,7(8):112.
［40］　HU X,ZHUANG D,ZHANG R,SUN X,LU Q,DAI Y.The small molecule inhibitor PR-619 protects retinal ganglion cells against glutamate excitotoxicity［J］．Neuroreport,2020,31(16):1134-1141.
［41］　WONG Y C,HOLZBAUR E L.Optineurin is an autophagy receptor for damaged mitochondria in parkin-mediated mitophagy that is disrupted by an ALS-linked mutation［J］．Proc Natl Acad Sci U S A,2014,111(42):e4439-e4448.
［42］　WONG Y C,HOLZBAUR E L.Temporal dynamics of PARK2/parkin and OPTN/optineurin recruitment during the mitophagy of damaged mitochondria［J］．Autophagy,2015,11(2):422-424.
［43］　CHERNYSHOVA K,INOUE K,YAMASHITA S I,FUKUCHI T,KANKI T.Glaucoma-associated mutations in the optineurin gene have limited impact on parkin-dependent mitophagy［J］．Invest Ophthalmol Vis Sci,2019,60(10):3625-3635.
［44］　HU X,DAI Y,ZHANG R,SHANG K,SUN X.Overexpression of optic atrophy type 1 protects retinal ganglion cells and upregulates parkin expression in experimental glaucoma［J］．Front Mol Neurosci,2018,11:350.
［45］　RATNAPRIYA R,CHEW E Y.Age-related macular degeneration-clinical review and genetics update［J］．Clin Genet,2013,84(2):160-166.
［46］　BLASIAK J,PAWLOWSKA E,SZCZEPANSKA J,KAARNIRANTA K.Interplay between autophagy and the ubiquitin-proteasome system and its role in the pathogenesis of age-related macular degeneration［J］．Int J Mol Sci,2019,20(1):210.
［47］　SKERKA C,LAUER N,WEINBERGER A A,KEILHAUER C N,SUHNEL J,SMITH R,et al.Defective complement control of factor H (Y402H) and FHL-1 in age-related macular degeneration［J］．Mol Immunol,2007,44(13):3398-3406.
［48］　MERLE D A,PROVENZANO F,JARBOUI M A,KILGER E,CLARK S J,DELEIDI M,et al.mTOR inhibition via rapamycin treatment partially reverts the deficit in energy metabolism caused by FH loss in RPE cells［J］．Antioxidants (Basel),2021,10(12):1944.
［49］　KAARNIRANTA K,SALMINEN A,ESKELINEN E L,KOPITZ J.Heat shock proteins as gatekeepers of proteolytic pathways-implications for age-related macular degeneration (AMD)［J］．Ageing Res Rev,2009,8(2):128-139.
［50］　SUBRIZI A,TOROPAINEN E,RAMSAY E,AIRAKSINEN A J,KAARNIRANTA K,URTTI A.Oxidative stress protection by exogenous delivery of rhHsp70 chaperone to the retinal pigment epithelium(RPE),a possible therapeutic strategy against RPE degeneration［J］．Pharm Res,2015,32(1):211-221.
［51］　ZHENG Q,HUANG C,GUO J,TAN J,WANG C,TANG B,et al.Hsp70 participates in PINK1-mediated mitophagy by regulating the stability of PINK1［J］．Neurosci Lett,2018,662:264-270.
［52］　SRIDEVI GURUBARAN I,VIIRI J,KOSKELA A,HYTTINEN J M T,PATERNO J J,KIS G,et al.Mitophagy in the retinal pigment epithelium of dry age-related macular degeneration investigated in the NFE2L2/PGC-1α-/- mouse model［J］．Int J Mol Sci,2020,21(6):1976.
［53］　DASKIVICH L P,VASQUEZ C,MARTINEZ C J,TSENG C H,MANGIONE C M.Implementation and evaluation of a large-scale teleretinal diabetic retinopathy screening program in the Los Angeles county department of health services［J］．JAMA Intern Med,2017,177(5):642-649.
［54］　SINGH L P,DEVI T S,YUMNAMCHA T.The role of TXNIP in mitophagy dysregulation and inflammasome activation in diabetic retinopathy:a new perspective［J］．JOJ Ophthalmol,2017,4(4):555643.
［55］　SPENGLER K,KRYEZIU N,GROBE S,MOSIG A S,HELLER R.VEGF triggers transient induction of autophagy in endothelial cells via AMPKα1［J］．Cells,2020,9(3):687.
［56］　PRADEEPKIRAN J A,REDDY P H.Defective mitophagy in Alzheimer’s disease［J］．Ageing Res Rev,2020,64:101191.
［57］　HOMBREBUENO J R,CAIRNS L,DUTTON L R,LYONS T J,BRAZIL D P,MOYNAGH P,et al.Uncoupled turnover disrupts mitochondrial quality control in diabetic retinopathy［J］．JCI Insight,2019,4(23):e129760.
［58］　ZHANG Y,XI X,MEI Y,ZHAO X,ZHOU L,MA M,et al.High-glucose induces retinal pigment epithelium mitochondrial pathways of apoptosis and inhibits mitophagy by regulating ROS/PINK1/Parkin signal pathway［J］．Biomed Pharmacother,2019,111:1315-1325.
［59］　HUANG C,LU H,XU J,YU H,WANG X,ZHANG X.Protective roles of autophagy in retinal pigment epithelium under high glucose condition via regulating PINK1/parkin pathway and BNIP3L［J］．Biol Res,2018,51(1):22.
［60］　XIE J,CUI Y,CHEN X,YU H,CHEN J,HUANG T,et al.VDAC1 regulates mitophagy in NLRP3 inflammasome activation in retinal capillary endothelial cells under high-glucose conditions［J］．Exp Eye Res,2021,209:108640.
［61］　ZHANG M Y,ZHU L,ZHENG X,XIE T H,WANG W,ZOU J,et al.TGR5 activation ameliorates mitochondrial homeostasis via regulating the PKCδ/Drp1-HK2 signaling in diabetic retinopathy［J］．Front Cell Dev Biol,2022,9:759421.
［62］　ZHOU P,XIE W,MENG X,ZHAI Y,DONG X,ZHANG X,et al.Notoginsenoside R1 ameliorates diabetic retinopathy through PINK1-dependent activation of mitophagy［J］．Cells,2019,8(3):213.
［63］　DOGANLAR Z B,DOGANLAR O,KURTDERE K,GUCLU H,CHASAN T,TURGUT E.Melatonin prevents blood-retinal barrier breakdown and mitochondrial dysfunction in high glucose and hypoxia-induced in vitro diabetic macular edema model［J］．Toxicol In Vitro,2021,75:105191.
［64］　ZHOU H R,MA X F,LIN W J,HAO M,YU X Y,LI H X,et al.Neuroprotective role of GLP-1 analog for retinal ganglion cells via PINK1/parkin-mediated mitophagy in diabetic retinopathy［J］．Front Pharmacol,2021,11:589114.
［65］　MA X,LIN W,LIN Z,HAO M,GAO X,ZHANG Y,et al.Liraglutide alleviates H2O2-induced retinal ganglion cells injury by inhibiting autophagy through mitochondrial pathways［J］．Peptides,2017,92:1-8.
［66］　ZHOU B,FANG L,DONG Y,YANG J,CHEN X,ZHANG N,et al.Mitochondrial quality control protects photoreceptors against oxidative stress in the H2O2-induced models of retinal degeneration diseases［J］．Cell Death Dis,2021,12(5):413.
［67］　ZHANG D,WU J,WU J,ZHANG S.Paeonol induces protective autophagy in retinal photoreceptor cells［J］．Front Pharmacol,2021,12:667959.
［68］　HUANG Z,REN S,JIANG Y,WANG T.PINK1 and parkin cooperatively protect neurons against constitutively active TRP channel-induced retinal degeneration in drosophila［J］．Cell Death Dis,2016,7(4):e2179.
［69］　WALLACE D C,LOTT M T.Leber hereditary optic neuropathy:exemplar of an mtDNA disease［J］．Handb Exp Pharmacol,2017,240:339-376.
［70］　ZHANG J,JI Y,LU Y,FU R,XU M,LIU X,et al.Leber’s hereditary optic neuropathy (LHON)-associated ND5 12338T>C mutation altered the assembly and function of complex I,apoptosis and mitophagy［J］．Hum Mol Genet,2018,27(11):1999-2011.
［71］　JI Y,NIE Z,MENG F,HU C,CHEN H,JIN L,et al.Mechanistic insights into mitochondrial tRNAAla 3’-end metabolism deficiency［J］．J Biol Chem,2021,297(1):100816.
［72］　ZHANG J,JI Y,CHEN J,XU M,WANG G,CI X,et al.Assocation between Leber’s hereditary optic neuropathy and MT-ND1 3460G>A mutation-induced alterations in mitochondrial function,apoptosis,and mitophagy［J］．Invest Ophthalmol Vis Sci,2021,62(9):38.

相似文献/References:

[1]蒙青青 刘苏.ROCK抑制剂在眼科基础及临床应用研究进展[J].眼科新进展,2013,33(9):000.
[2]杜宇翔,郭大东,毕宏生. 视觉系统中钙库操纵钙内流通路的研究进展[J].眼科新进展,2014,34(4):389.[doi:10.13389/j.cnki.rao.2014.0108]
[3]宋惠欣,吴建峰,毕宏生.表皮生长因子在眼科疾病中的作用[J].眼科新进展,2017,37(5):484.[doi:10.13389/j.cnki.rao.2017.0123]
　SONG Hui-Xin,WU Jian-Feng,BI Hong-Sheng.Role of epidermal growth factor in ocular diseases[J].Recent Advances in Ophthalmology,2017,37(3):484.[doi:10.13389/j.cnki.rao.2017.0123]
[4]徐婷婷,邵毅,周琼.泪液标志物在系统性疾病中的研究进展[J].眼科新进展,2017,37(8):780.[doi:10.13389/j.cnki.rao.2017.0198]
　XU Ting-Ting,SHAO Yi,ZHOU Qiong.Recent progression on tear fluid markers in systemic disease[J].Recent Advances in Ophthalmology,2017,37(3):780.[doi:10.13389/j.cnki.rao.2017.0198]
[5]刘滨,郭大东,孙园园,等.自噬调控眼部疾病进程的研究进展[J].眼科新进展,2017,37(8):797.[doi:10.13389/j.cnki.rao.2017.0202]
　LIU Bin,GUO Da-Dong,SUN Yuan-Yuan,et al.Recent advances in regulation of autophagy in ocular diseases[J].Recent Advances in Ophthalmology,2017,37(3):797.[doi:10.13389/j.cnki.rao.2017.0202]
[6]管丽红,林俊堂.CRISPR-Cas9基因编辑技术在眼科疾病中的应用[J].眼科新进展,2018,38(9):801.[doi:10.13389/j.cnki.rao.2018.0190]
　GUAN Li-Hong,LIN Jun-Tang.Application of CRISPR-Cas9 technology in ophthalmological diseases[J].Recent Advances in Ophthalmology,2018,38(3):801.[doi:10.13389/j.cnki.rao.2018.0190]
[7]柴广睿,刘姝,陈晓隆.核苷酸结合寡聚化结构域样受体蛋白3（NLRP3）炎症体在眼科疾病中的研究进展[J].眼科新进展,2018,38(9):892.[doi:10.13389/j.cnki.rao.2018.0211]
　CHAI Guang-Rui,LIU Shu,CHEN Xiao-Long.The progress of NLRP3 inflammasome in ophthalmic diseases[J].Recent Advances in Ophthalmology,2018,38(3):892.[doi:10.13389/j.cnki.rao.2018.0211]
[8]容蓉,鲍静,邵毅.偏振光学相干断层成像技术在临床眼科疾病中的应用[J].眼科新进展,2018,38(9):898.[doi:10.13389/j.cnki.rao.2018.0212]
　RONG Rong,BAO Jing,SHAO Yi.Application of polarization sensitive optical coherence tomography in clinical ophthalmic diseases[J].Recent Advances in Ophthalmology,2018,38(3):898.[doi:10.13389/j.cnki.rao.2018.0212]
[9]孙姣,王佳琳,王艳玲,等.眼部血管密度测量及其临床意义研究进展[J].眼科新进展,2018,38(11):1089.[doi:10.13389/j.cnki.rao.2018.0257]
　SUN Jiao,WANG Jia-Lin,WANG Yan-Ling,et al.Research progress of vessel density in ocular diseases[J].Recent Advances in Ophthalmology,2018,38(3):1089.[doi:10.13389/j.cnki.rao.2018.0257]
[10]陈熹,陈水莲,余克明,等.外泌体及其与眼科疾病的免疫学关系[J].眼科新进展,2019,39(11):1087.[doi:10.13389/j.cnki.rao.2019.0250]
　CHEN Xi,CHEN Shui-Lian,YU Ke-Ming,et al.Immunological relationship between exosomes and ophthalmic diseases[J].Recent Advances in Ophthalmology,2019,39(3):1087.[doi:10.13389/j.cnki.rao.2019.0250]

备注/Memo

备注/Memo:
国家自然科学基金资助（编号：81770906，81974129，8217 1038）
更新日期/Last Update: 2023-03-05