细胞焦亡在眼部疾病中的研究进展
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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。
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 nonbacterial 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.
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 nonbacterial 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.
引文
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[5]BROZ P.Immunology:Caspase target drives pyroptosis[J].Nature,2015,526(7575):642-643.
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[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.
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[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,SI-VAK 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,GREGO-RY 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 RNAKCNQ1OT1 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,VAVVASD 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.
[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,WUH,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 AP.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-VEGFtherapies 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-ASABM,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,SI-VAK 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,GREGO-RY 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 RNAKCNQ1OT1 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,VAVVASD 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.