Caspase家族与干眼症的研究进展

doi:10.3760/cma.j.cn115909-20200320-00107

摘要
图/表
参考文献(47)
相关文章 (15)

全文: PDF 733KB HTML (1 KB)
输出: BibTeX | EndNote (RIS) 背景资料

文章导读

摘要 Caspase家族是一类同源天冬氨酸特异性半胱氨酸蛋白酶，它们级联活化后降解其产物，参与炎症因子的产生以及细胞凋亡的调节。干眼症是眼科的常见疾病，是一种多因素相互作用所致的一种眼表疾病。细胞凋亡在干眼症的发病机制中占有非常重要的地位，炎症反应也被证实在干眼症的发病机制中发挥重要作用。近年来，人们对Caspase家族的分子机制及其在干眼症的发病机制有了较为深度的认识。这些研究为干眼症的发病机制及治疗提供新的思路。笔者将对Caspase的分子结构和特征及其在干眼症中的作用进行综述。

	服务

	把本文推荐给朋友
	加入我的书架
	加入引用管理器
	E-mail Alert
	RSS
	作者相关文章

关键词 ： , 干眼症, 细胞凋亡, 细胞焦亡, Caspase

Abstract： Caspases are a family of cysteine-containing aspartate-specific proteases, hydrolyze their substrates after cascade activation, that involved in apoptosis and inflammation responses. Dry eye disease is a common ocular disease caused by multiple factors. Apoptosis plays a very important role in the pathogenesis of dry eye disease, and inflammation has also been confirmed to play an important role in the pathogenesis of dry eye disease. In recent years, the molecular mechanism of the Caspase family and its pathogenesis in dry eye disease have been well understood. These researches provide new insights for the pathogenesis and treatment of dry eye disease. This article will review the molecular structure and characteristics of Caspase and its role in dry eye disease.

Key words： dry eye disease apoptosis pyroptosis Caspase

收稿日期: 2020-03-20

PACS:

基金资助: 浙江省重大科技项目（2017C03046）

通讯作者: 徐雯（ORCID：0000-0002-6277-7136），Email：xuwen2003@zju.edu.cn

引用本文:

吴星镝徐雯. Caspase家族与干眼症的研究进展[J]. 中华眼视光学与视觉科学杂志, 2021, 23(7): 546-551. Xingdi Wu, Wen Xu. Research Progress of Caspase and Dry Eye Disease. Chinese Journal of Optometry Ophthalmology and Visual science, 2021, 23(7): 546-551. DOI: 10.3760/cma.j.cn115909-20200320-00107

链接本文:

https://www.cjoovs.com/CN/10.3760/cma.j.cn115909-20200320-00107 或 https://www.cjoovs.com/CN/Y2021/V23/I7/546

[1]	刘祖国, 王华. 关注干眼慢性疾病管理体系的建设. 中华眼科杂志, 2018, 54(2): 81-83. DOI: 10.3760/cma.j.issn.0412-4081. 2018.02.001.
[2]	Craig JP, Nichols KK, Akpek EK, et al. TFOS DEWS II Definition and Classification Report. Ocul Surf, 2017, 15(3): 276-283. DOI: 10.1016/j.jtos.2017.05.008.
[3]	Yamaguchi T. Inflammatory response in dry eye. Invest Ophthalmol Vis Sci, 2018, 59(14): DES192-DES199. DOI: 10.1167/iovs.17-23651.
[4]	Rhee MK, Mah FS. Inflammation in dry eye disease: How do we break the cycle? Ophthalmology, 2017, 124(11S): S14-S19. DOI: 10.1016/j.ophtha.2017.08.029.
[5]	Ramirez MLG, Salvesen GS. A primer on caspase mechanisms. Semin Cell Dev Biol, 2018, 82: 79-85. DOI: 10.1016/j.semcdb. 2018.01.002.
[6]	Vande Walle L, Lamkanfi M. Pyroptosis. Curr Biol, 2016, 26(13): R568-R572. DOI: 10.1016/j.cub.2016.02.019.
[7]	Lamkanfi M, Declercq W, Kalai M, et al. Alice in caspase land. A phylogenetic analysis of caspases from worm to man. Cell Death Differ, 2002, 9(4): 358-361. DOI: 10.1038/ sj.cdd.4400989.
[8]	Riedl SJ, Salvesen GS. The apoptosome: Signalling platform of cell death. Nat Rev Mol Cell Biol, 2007, 8(5): 405-413. DOI: 10.1038/nrm2153.
[9]	Dickens LS, Boyd RS, Jukes-Jones R, et al. A death effector domain chain DISC model reveals a crucial role for Caspase-8chain assembly in mediating apoptotic cell death. Mol Cell, 2012, 47(2): 291-305. DOI: 10.1016/j.molcel.2012.05.004.
[10]	Shamas-Din A, Bindner S, Zhu W, et al. tBid undergoes multiple conformational changes at the membrane required for Bax activation. J Biol Chem, 2013, 288(30): 22111-22127. DOI: 10.1074/jbc.M113.482109.
[11]	Horn S, Hughes MA, Schilling R, et al. Caspase-10 negatively regulates Caspase-8-mediated cell death, switching the response to CD95L in favor of NF-κB activation and cell survival. Cell Rep, 2017, 19(4): 785-797. DOI: 10.1016/ j.celrep.2017.04.010
[12]	Lamy L, Ngo VN, Emre NC, et al. Control of autophagic cell death by Caspase-10 in multiple myeloma. Cancer Cell, 2013, 23(4): 435-449. DOI: 10.1016/j.ccr.2013.02.017.
[13]	Li LY, Luo X, Wang X. Endonuclease G is an apoptotic DNase when released from mitochondria. Nature, 2001, 412(6842): 95- 99. DOI: 10.1038/35083620.
[14]	Jan Y, Matter M, Pai JT, et al. A mitochondrial protein, Bit1, mediates apoptosis regulated by integrins and Groucho/TLE corepressors. Cell, 2004, 116(5): 751-762. DOI: 10.1016/s0092- 8674(04)00204-1.
[15]	Pop C, Timmer J, Sperandio S, et al. The apoptosome activates Caspase-9 by dimerization. Mol Cell, 2006, 22(2): 269-275. DOI: 10.1016/j.molcel.2006.03.009.
[16]	Yu X, Wang L, Acehan D, et al. Three-dimensional structure of a double apoptosome formed by the Drosophila Apaf-1 related killer. J Mol Biol, 2006, 355(3): 577-589. DOI: 10.1016/ j.jmb.2005.10.040.
[17]	Van Opdenbosch N, Lamkanfi M. Caspases in cell death, inflammation, and disease. Immunity, 2019, 50(6): 1352-1364. DOI: 10.1016/j.immuni.2019.05.020.
[18]	Fink SL, Cookson BT. Apoptosis, pyroptosis, and necrosis: Mechanistic description of dead and dying eukaryotic cells. Infect Immun, 2005, 73(4): 1907-1916. DOI: 10.1128/iai.73.4. 1907-1916.2005.
[19]	Jorgensen I, Rayamajhi M, Miao EA. Programmed cell death as a defence against infection. Nat Rev Immunol, 2017, 17(3): 151- 164. DOI: 10.1038/nri.2016.147.
[20]	Schneider KS, Gros CJ, Dreier RF, et al. The inflammasome drives GSDMD-independent secondary pyroptosis and IL-1 release in the absence of Caspase-1 protease activity. Cell Rep, 2017, 21(13): 3846-3859. DOI: 10.1016/j.celrep.2017.12.018.
[21]	Yazdi AS, Guarda G, D'Ombrain MC, et al. Inflammatory Caspases in innate immunity and inflammation. J Innate Immun, 2010, 2(3): 228-237. DOI: 10.1159/000283688.
[22]	Kayagaki N, Stowe IB, Lee BL, et al. Caspase-11 cleaves gasdermin D for non-canonical inflammasome signalling. Nature, 2015, 526(7575): 666-671. DOI: 10.1038/nature15541.
[23]	Schroder K, Tschopp J. The inflammasomes. Cell, 2010, 140(6): 821-832. DOI: 10.1016/j.cell.2010.01.040.
[24]	Yuan J, Najafov A, Py BF. Roles of Caspases in necrotic cell death. Cell, 2016, 167(7): 1693-1704. DOI: 10.1016/ j.cell.2016.11.047.
[25]	Kayagaki N, Warming S, Lamkanfi M, et al. Non-canonical inflammasome activation targets caspase-11. Nature, 2011, 479(7371): 117-121. DOI: 10.1038/nature10558.
[26]	Pflugfelder SC, de Paiva CS. The Pathophysiology of dry eye disease: What we know and future directions for research. Ophthalmology, 2017, 124(11S): S4-S13. DOI: 10.1016/ j.ophtha.2017.07.010.
[27]	Yeh S, Song XJ, Farley W, et al. Apoptosis of ocular surface cells in experimentally induced dry eye. Invest Ophthalmol Vis Sci, 2003, 44(1): 124-129. DOI: 10.1167/iovs.02-0581.
[28]	Zhang X, Chen W, De Paiva CS, et al. Interferon-gamma exacerbates dry eye-induced apoptosis in conjunctiva through dual apoptotic pathways. Invest Ophthalmol Vis Sci, 2011, 52(9): 6279-6285. DOI: 10.1167/iovs.10-7081.
[29]	Zhang X, Chen W, De Paiva CS, et al. Desiccating stress induces CD4+ T-cell-mediated Sjögren's syndrome-like corneal epithelial apoptosis via activation of the extrinsic apoptotic pathway by interferon-γ. Am J Pathol, 2011, 179(4): 1807-1814. DOI: 10.1016/j.ajpath.2011.06.030.
[30]	Brignole F, De Saint-Jean M, Goldschild M, et al. Expression of Fas-Fas ligand antigens and apoptotic marker APO2.7 by the human conjunctival epithelium. Positive correlation with class II HLA DR expression in inflammatory ocular surface disorders. Exp Eye Res, 1998, 67(6): 687-697. DOI: 10.1006/ exer.1998.0566.
[31]	Brignole F, Pisella PJ, Goldschild M, et al. Flow cytometric analysis of inflammatory markers in conjunctival epithelial cells of patients with dry eyes. Invest Ophthalmol Vis Sci, 2000, 41(6): 1356-1363.
[32]	Brignole F, Pisella P J, De Saint Jean M, et al. Flow cytometric analysis of inflammatory markers in KCS: 6-month treatment with topical cyclosporin A. Invest Ophthalmol Vis Sci, 2001, 42(1): 90-95.
[33]	Yoshida A, Fujihara T, Nakata K. Cyclosporin A increases tear fluid secretion via release of sensory neurotransmitters and muscarinic pathway in mice. Exp Eye Res, 1999, 68(5): 541- 546. DOI: 10.1006/exer.1998.0619.
[34]	Chi W, Hua X, Chen X, et al. Mitochondrial DNA oxidation induces imbalanced activity of NLRP3/NLRP6 inflammasomes by activation of caspase-8 and BRCC36 in dry eye. J Autoimmun, 2017, 80: 65-76. DOI: 10.1016/j.jaut.2017.02.006.
[35]	Strong B, Farley W, Stern M E, et al. Topical cyclosporine inhibits conjunctival epithelial apoptosis in experimental murine keratoconjunctivitis sicca. Cornea, 2005, 24(1): 80-85. DOI: 10.1097/01.ico.0000133994.22392.47.
[36]	Wehner F, Olsen H, Tinel H, et al. Cell volume regulation: osmolytes, osmolyte transport, and signal transduction. Rev Physiol Biochem Pharmacol, 2003, 148: 1-80. DOI: 10.1007/ s10254-003-0009-x.
[37]	Chen W, Zhang X, Li J, et al. Efficacy of osmoprotectants on prevention and treatment of murine dry eye. Invest Ophthalmol Vis Sci, 2013, 54(9): 6287-6297. DOI: 10.1167/iovs.13-12081.
[38]	Wu Y, Bu J, Yang Y, et al. Therapeutic effect of MK2 inhibitor on experimental murine dry eye. Invest Ophthalmol Vis Sci, 2017, 58(11): 4898-4907. DOI: 10.1167/iovs.17-22240.
[39]	Bulosan M, Pauley KM, Yo K, et al. Inflammatory caspases are critical for enhanced cell death in the target tissue of Sjögren's syndrome before disease onset. Immunol Cell Biol, 2009, 87(1): 81-90. DOI: 10.1038/icb.2008.70.
[40]	Im H, Ammit AJ. The NLRP3 inflammasome: Role in airway inflammation. Clin Exp Allergy, 2014, 44(2): 160-172. DOI: 10.1111/cea.12206.
[41]	Kahlenberg JM, Kaplan MJ. The inflammasome and lupus: Another innate immune mechanism contributing to disease pathogenesis? Curr Opin Rheumatol, 2014, 26(5): 475-481. DOI: 10.1097/bor.0000000000000088.
[42]	Yerramothu P, Vijay AK, Willcox M. Inflammasomes, the eye and anti-inflammasome therapy. Eye (Lond), 2018, 32(3): 491- 505. DOI: 10.1038/eye.2017.241.
[43]	Baldini C, Rossi C, Ferro F, et al. The P2X7 receptor-inflammasome complex has a role in modulating the inflammatory response in primary Sjögren's syndrome. J Intern Med, 2013, 274(5): 480-489. DOI: 10.1111/joim.12115.
[44]	Niu L, Zhang S, Wu J, et al. Upregulation of NLRP3 inflammasome in the tears and ocular surface of dry eye patients. PLoS One, 2015, 10(5): e0126277. DOI: 10.1371/ journal.pone.0126277.
[45]	Zheng Q, Ren Y, Reinach PS, et al. Reactive oxygen species activated NLRP3 inflammasomes prime environment-induced murine dry eye. Exp Eye Res, 2014, 125: 1-8. DOI: 10.1016/ j.exer.2014.05.001.
[46]	Zheng Q, Ren Y, Reinach PS, et al. Reactive oxygen species activated NLRP3 inflammasomes initiate inflammation in hyperosmolarity stressed human corneal epithelial cells and environment-induced dry eye patients. Exp Eye Res, 2015, 134: 133-140. DOI: 10.1016/j.exer.2015.02.013.
[47]	Dai Y, Zhang J, Xiang J, et al. Calcitriol inhibits ROS-NLRP3- IL-1β signaling axis via activation of Nrf2-antioxidant signaling in hyperosmotic stress stimulated human corneal epithelial cells. Redox Biol, 2019, 21: 101093. DOI: 10.1016/ j.redox.2018.101093.