[1]张敏,李志坚,王亚敏.细胞焦亡在眼部疾病中的研究进展[J].眼科新进展,2019,39(1):082-85.[doi:10.13389/j.cnki.rao.2019.0019]
 ZHANG Min,LI Zhi-Jian,WANG Ya-Min.Research progress of pyroptosis in ocular diseases[J].Recent Advances in Ophthalmology,2019,39(1):082-85.[doi:10.13389/j.cnki.rao.2019.0019]
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细胞焦亡在眼部疾病中的研究进展/HTML
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《眼科新进展》[ISSN:1003-5141/CN:41-1105/R]

卷:
39卷
期数:
2019年1期
页码:
082-85
栏目:
文献综述
出版日期:
2019-01-05

文章信息/Info

Title:
Research progress of pyroptosis in ocular diseases
作者:
张敏李志坚王亚敏
150001 黑龙江省哈尔滨市,哈尔滨医科大学附属第一医院眼科医院
Author(s):
ZHANG MinLI Zhi-JianWANG Ya-Min
Eye Hospital,the First Affiliated Hospital of Harbin Medical University,Harbin 150001,Heilongjiang Province,China
关键词:
细胞焦亡老年性黄斑变性角膜炎白内障
Keywords:
pyroptosisage-related macular degenerationkeratitiscataract
分类号:
R77
DOI:
10.13389/j.cnki.rao.2019.0019
文献标志码:
A
摘要:
细胞焦亡与细胞凋亡、细胞坏死及自噬不同,是一种程序性促炎性细胞死亡方式。其主要信号通路包括依赖caspase-1的经典焦亡途径和依赖caspase-4/5、caspase-11的非经典焦亡途径。已有大量研究表明,细胞焦亡与感染性疾病、动脉粥样硬化性疾病、代谢性疾病及重要脏器非细菌性炎性疾病相关。近几年细胞焦亡在眼部疾病中也有部分研究,包括老年性黄斑变性、角膜炎、白内障等疾病。本文主要综述细胞焦亡的主要机制及其在眼部疾病中的研究进展。
Abstract:
Pyroptosis is a programmed pro-inflammatory cell death mode which different from apoptosis,necrosis and autophagy.The main signaling pathways include classic caspase-1-dependent pyroptosis and non-classical caspase-4/5-dependent and caspase-11 dependent pyroptosis.A large number of studies have shown that pyroptosis is associated with infectious diseases,atherosclerotic diseases,metabolic diseases and important non-bacterial inflammatory diseases of organs.In recent years,pyroptosis has been studied in some eye disease,including age-related macular degeneration,keratitis,cataract and other diseases.The main mechanism of pyroptosis and its progress in ocular diseases will be reviewed in this paper.

参考文献/References:

[1] FINK S L,COOKSON B T.Apoptosis,pyroptosis,and necrosis:mechanistic description of dead and dying eukaryotic cells[J].Infect Immun,2005,73(4):1907-1916.
[2] BERGSBAKEN T,FINK S L,COOKSON B T.Pyroptosis:host cell death and inflammation[J].Nat Rev Microbiol,2009,7(2):99-109.
[3] CHEN X,HE W T,HU L,LI J,FANG Y,WANG X,et al.Pyroptosis is driven by non-selective gasdermin-D pore and its morphology is different from MLKL channel-mediated necroptosis[J].Cell Res,2016,26(9):1007-1020.
[4] MAN S M,KANNEGANTI T D.Gasdermin D:the long-awaited executioner of pyroptosis[J].Cell Res,2015,25(11):1183-1184.
[5] BROZ P.Immunology:Caspase target drives pyroptosis[J].Nature,2015,526(7575):642-643.
[6] MARTINON F,BURNS K,TSCHOPP J.The inflammasome:a molecular platform triggering activation of inflammatory caspases and processing of proIL-beta[J].Mol Cell,2002,10(2):417-426.
[7] DING J,WANG K,LIU W,SHE Y,SUN Q,SHI J,et al.Erratum:Pore-forming activity and structural autoinhibition of the gasdermin family[J].Nature,2016,535(7610):111-116.
[8] LIU X,ZHANG Z,RUAN J,PAN Y,MAGUPALLI V G,WU H,et al.Inflammasome-activated gasdermin D causes pyroptosis by forming membrane pores[J].Nature,2016,535(7610):153-158.
[9] DUNAIEF J L,DENTCHEV T,YING G S,MILAM AH.The role of apoptosis in age-related macular degeneration[J].Arch Ophthalmol,2002,120(11):1435-1442.
[10] AMBATI J,AMBATI B K,Yoo S H,LANCHULEV S,ADAMIS A P.Age-related macular degeneration:etiology,pathogenesis,and therapeutic strategies[J].Surv Ophthalmol,2003,48(3):257-293.
[11] AMOAKU W M,CHAKRAVARTHY U,GALE R,GAVIN M,CHANCHI F,GIBSON J,et al.Defining response to anti-VEGF therapies in neovascular AMD[J].Eye (Lond),2015,29(6):721-731.
[12] SINGH M,TYAGI S C.Hyperhomocysteinemia and age-related macular degeneration:role of inflammatory mediators and pyroptosis:a Proposal[J].Med Hypotheses,2017,105:17-21.
[13] CHEN S,SHEN D,POPP N A,OGILVY A J,TUO J,ABU-ASAB M,et al.Responses of Multipotent Retinal Stem Cells to IL-1β,IL-18,or IL-17[J].J Ophthalmol,2015,2015:369312.
[14] GAO J,CUI J Z,TO E,CAO S,MATSUBARA J A.Evidence for the activation of pyroptotic and apoptotic pathways in RPE cells associated with NLRP3 inflammasome in the rodent eye[J].J Neuroinflammat,2018,15(1):15.
[15] VIRINGIPURAMPEER I A,METCALFE A L,BASHAR A E,SIVAK O,YANAI A,MOHAMMADI Z,et al.NLRP3 inflammasome activation drives bystander cone photoreceptor cell death in a P23H rhodopsin model of retinal degeneration[J].Hum Mol Genet,2016,25(8):1501-1516.
[16] TSENG W A,THEIN T,KINNUNEN K,LASHKARI K,GREGORY M S,D’AMORE,P A,et al.NLRP3 inflammasome activation in retinal pigment epithelial cells by lysosomal destabilization:implications for age-related macular degeneration[J].Invest Ophthalmol Vis Sci,2013,54(1):110-120.
[17] BRANDSTETTER C,PATT J,HOLZ F G,KROHNE T U.Inflammasome priming increases retinal pigment epithelial cell susceptibility to lipofuscin phototoxicity by changing the cell death mechanism from apoptosis to pyroptosis[J].J Photochem Photobiol B,2016,161:177-183.
[18] JIN X,JIN H,SHI Y,GUO Y,ZHANG H.Pyroptosis,a novel mechanism implicated in cataracts[J].Mol Med Rep,2018,18(2):2277-2285.
[19] JIN X,JIN H,SHI Y,GUO Y,ZHANG H.Long non-coding RNA KCNQ1OT1 promotes cataractogenesis via miR-214 and activation of the caspase-1 pathway[J].Cell Physiol Biochem,2017,42(1):295-305.
[20] QU W,WANG Y,WU Y,LIU Y,CHEN K,ZOU Z,et al.Triggering receptors expressed on myeloid cells 2 promotes corneal resistance against by inhibiting caspase-1-dependent pyroptosis[J].Front Immunol,2018,9:1121.
[21] BRICKER-ANTHONY C,HINES-BEARD J,REX TS.Molecular changes and vision loss in a mouse model of closed-globe blast trauma[J].Invest Ophthalmol Vis Sci,2014,55(8):4853-4862.
[22] KIM L A,AMARNANI D,GNANAGURU G,TSENG W A,VAVVAS D G,D’AMORE,P A.Tamoxifen toxicity in cultured retinal pigment epithelial cells is mediated by concurrent regulated cell death mechanisms[J].Invest Ophthalmol Vis Sci,2014,55(8):4747-4758.

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备注/Memo

备注/Memo:
国家自然科学基金面上项目(编号:81870643)
更新日期/Last Update: 2019-01-04