中国医科大学学报

中国医科大学学报
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中国医科大学学报 ›› 2018, Vol. 47 ›› Issue (4): 358-363.doi: 10.12007/j.issn.0258-4646.2018.04.016

• 综述 • 上一篇    下一篇

线粒体功能障碍与年龄相关性眼部疾病的关系

李晓彤, 秦宇, 赵江月, 张劲松   

  1. 中国医科大学附属第四医院眼科, 中国医科大学眼科医院, 辽宁省晶状体学重点实验室, 沈阳 110005
  • 收稿日期:2017-07-11 出版日期:2018-04-30 发布日期:2018-04-10
  • 通讯作者: 张劲松 E-mail:cmu4h-zjs@126.com
  • 作者简介:李晓彤(1991-),女,硕士研究生.
  • 基金资助:
    国家自然科学基金(81470617,81270988,81371003,81600717);辽宁省自然科学基金(201602851)

Mitochondrial Dysfunction in Age-related Eye Disorders

LI Xiaotong, QIN Yu, ZHAO Jiangyue, ZHANG Jinsong   

  1. Department of Ophthalmology, The Fourth Affiliated Hospital, China Medical University, Eye Hospital of China Medical University, Key Lens Research Laboratory of Liaoning Province, Shenyang 110005, China
  • Received:2017-07-11 Online:2018-04-30 Published:2018-04-10

摘要: 线粒体是维持细胞功能及生存的关键细胞器,具有提供能量,调节细胞代谢、分化和控制细胞凋亡等重要作用。遗传性线粒体基因突变及氧化损伤所致线粒体损伤的逐步累积是导致疾病发生发展的重要因素。线粒体功能障碍与年龄相关性眼病,如糖尿病性视网膜病变、年龄相关性黄斑变性、青光眼、白内障等的发生密切相关。本文对年龄相关性疾病中线粒体发生功能障碍的相关生物学特点进行了综述,并简单总结了其与相应眼科疾病的关系。

关键词: 线粒体, 线粒体基因, 氧化应激, 活性氧

Abstract: Mitochondria are critical for ocular function as they represent the primary source of energy for cells,and play important roles in cell differentiation and survival. The etiology of many common disorders is recognized to involve either mitochondrial DNA mutations, or the gradual accumulation of mitochondrial damage caused by oxidative stress. Mitochondrial dysfunction is also being increasingly implicated in age-related eye disorders,including diabetic retinopathy,age-related macular degeneration,glaucoma,and cataract. In this review,we summarize the biological characteristics of mitochondrial dysfunction in age-related diseases,and their relationship to the corresponding ophthalmic diseases.

Key words: mitochondria, mitochondrial deoxyribonucleic acid, oxidative stress, reactive oxygen species

中图分类号: 

  • R77
[1] FALK MJ. Neurodevelopmental manifestations of mitochondrial disease[J]. J Dev Behav Pediatr,2010,31(7):610-621. DOI:10.1097/DBP.0b013e3181ef42c1.
[2] GRIMM A,ECKERT A. Brain aging and neurodegeneration:from a mitochondrial point of view[J]. J Neurochem,2017,143(4):418-431. DOI:10.1111/jnc.14037.
[3] GRIMM A,FRIEDLAND K,ECKERT A. Mitochondrial dysfunction:the missing link between aging and sporadic Alzheimer's disease[J]. Biogerontology,2016,17(2):281-296. DOI:10.1007/s10522-015-9618-4.
[4] SEO DY,LEE SR,KIM N,et al. Age-related changes in skeletal muscle mitochondria:the role of exercise[J]. Integr Med Res,2016,5(3):182-186. DOI:10.1016/j.imr.2016.07.003.
[5] HEPPLE RT. Impact of aging on mitochondrial function in cardiac and skeletal muscle[J]. Free Radic Biol Med,2016,98:177-186. DOI:10.1016/j.freeradbiomed.2016.03.017.
[6] ZHAO D,YANG J,YANG L. Insights for oxidative stress and mtor signaling in myocardial ischemia/reperfusion injury under diabetes[J]. Oxid Med Cell Longev,2017,2017:6437467. DOI:10.1155/2017/6437467.
[7] DYMKOWSKA D. Oxidative damage of the vascular endothelium in type 2 diabetes -the role of mitochondria and NAD (P) H oxidase[J]. Postepy Biochem,2016,62(2):116-126.
[8] OHIA SE,OPERE CA,LEDAY AM. Pharmacological consequences of oxidative stress in ocular tissues[J]. Mutat Res,2005,579(1/2):22-36. DOI:10.1016/j.mrfmmm.2005.03.025.
[9] NJIE-MBYE YF,KULKARNI-CHITNIS M,OPERE CA,et al. Lipid peroxidation:pathophysiological and pharmacological implications in the eye[J]. Front Physiol,2013,4:366. DOI:10.3389/fphys.2013.00366.
[10] NITA M,GRZYBOWSKI A. The role of the reactive oxygen species and oxidative stress in the pathomechanism of the age-related ocular diseases and other pathologies of the anterior and posterior eye segments in adults[J]. Oxid Med Cell Longev,2016,2016:3164734. DOI:10.1155/2016/3164734.
[11] KRUK J,KUBASIK-KLADNA K,ABOUL-ENEIN HY. The role oxidative stress in the pathogenesis of eye diseases:current status and a dual role of physical activity[J]. Mini Rev Med Chem,2015,16(3):241-257.
[12] LERUEZ S,AMATI-BONNEAU P,VERNY C,et al. Mitochondrial dysfunction affecting visual pathways[J]. Rev Neurol (Paris), 2014,170(5):344-354. DOI:10.1016/j.neurol.2014.03.009.
[13] APPELHANS T,RICHTER CP,WILKENS V,et al. Nanoscale organization of mitochondrial microcompartments revealed by combining tracking and localization microscopy[J]. Nano Lett,2012,12(2):610-616. DOI:10.1021/nl203343a.
[14] BUSCH KB,DECKERS-HEBESTREIT G,HANKE GT,et al. Dynamics of bioenergetic microcompartments[J]. Biol Chem,2013, 394(2):163-188. DOI:10.1515/hsz-2012-0254.
[15] DUDKINA NV,FOLEA IM,BOEKEMA EJ. Towards structural and functional characterization of photosynthetic and mitochondrial supercomplexes[J]. Micron,2015,72:39-51. DOI:10.1016/j.micron.2015.03.002.
[16] ATTARDI G,SCHATZ G. Biogenesis of mitochondria[J]. Annu Rev Cell Biol,1988,4:289-333. DOI:10.1146/annurev.cb.04.110188.001445.
[17] SHAFA SHARIAT PANAHI M,HOUSHMAND M,TABASSI AR. Mitochondrial D-loop variation in leber hereditary neuropathy patients harboring primary G11778A,G3460A,T14484C mutations:J and W haplogroups as high-risk factors[J]. Arch Med Res,2006,37(8):1028-1033. DOI:10.1016/j.arcmed.2006.04.009.
[18] REZVANI Z,DIDARI E,ARASTEHKANI A,et al. Fifteen novel mutations in the mitochondrial NADH dehydrogenase subunit 1,2, 3,4,4L,5 and 6 genes from Iranian patients with Leber's hereditary optic neuropathy (LHON)[J]. Mol Biol Rep,2013,40(12):6837-6841. DOI:10.1007/s11033-013-2801-2.
[19] YAKES FM,VAN HOUTEN B. Mitochondrial DNA damage is more extensive and persists longer than nuclear DNA damage in human cells following oxidative stress[J]. Proc Natl Acad Sci USA,1997, 94(2):514-519.
[20] BLASIAK J,GLOWACKI S,KAUPPINEN A,et al. Mitochondrial and nuclear DNA damage and repair in age-related macular degeneration[J]. Int J Mol Sci,2013,14(2):2996-3010. DOI:10.3390/ijms14022996.
[21] BLASIAK J,SZAFLIK JP. DNA damage and repair in age-related macular degeneration[J]. Front Biosci (Landmark Ed),2011,16:1291-1301.
[22] JARRETT SG,BOULTON ME. Poly (ADP-ribose) polymerase offers protection against oxidative and alkylation damage to the nuclear and mitochondrial genomes of the retinal pigment epithelium[J]. Ophthalmic Res,2007,39(4):213-223. DOI:10.1159/000104683.
[23] KOVACS K,ERDELYI K,HEGEDUS C,et al. Poly (ADP-ribosyl) ation is a survival mechanism in cigarette smoke-induced and hydrogen peroxide-mediated cell death[J]. Free Radic Biol Med,2012,53(9):1680-1688. DOI:10.1016/j.freeradbiomed.2012.08.579.
[24] WANG K,TAKAHASHI Y,GAO ZL,et al. Mitochondrial ND3 as the novel causative gene for Leber hereditary optic neuropathy and dystonia[J]. Neurogenetics,2009,10(4):337-345. DOI:10.1007/s10048-009-0194-0.
[25] BALLARD JW,KATEWA SD,MELVIN RG,et al. Comparative analysis of mitochondrial genotype and aging[J]. Ann N Y Acad Sci,2007,1114:93-106. DOI:10.1196/annals.1396.011.
[26] MITCHELL P. Coupling of phosphorylation to electron and hydrogen transfer by a chemi-osmotic type of mechanism[J]. Nature,1961, 191:144-148.
[27] AGARONYAN K,MOROZOV YI,ANIKIN M,et al. Mitochondrial biology. Replication-transcription switch in human mitochondria[J]. Science,2015,347(6221):548-551. DOI:10.1126/science. aaa0986.
[28] YUM HR,CHAE H,SHIN SY,et al. Pathogenic mitochondrial DNA mutations and associated clinical features in Korean patients with Leber's hereditary optic neuropathy[J]. Invest Ophthalmol Vis Sci, 2014,55(12):8095-8101. DOI:10.1167/iovs.14-15311.
[29] PATRUSHEV MV,MAZUNIN IO,VINOGRADOVA EN,et al. Mitochondrial fission and fusion[J]. Biochemistry (Mosc),2015,80(11):1457-1464. DOI:10.1134/S0006297915110061.
[30] MALKA F,GUILLERY O,CIFUENTES-DIAZ C,et al. Separate fusion of outer and inner mitochondrial membranes[J]. EMBO Rep, 2005,6(9):853-859. DOI:10.1038/sj.embor.7400488.
[31] SILVA RAMOS E,LARSSON NG,MOURIER A. Bioenergetic roles of mitochondrial fusion[J]. Biochim Biophys Acta,2016,1857(8):1277-1283. DOI:10.1016/j.bbabio.2016.04.002.
[32] BIRCH-MACHIN MA,BOWMAN A. Oxidative stress and ageing[J]. Br J Dermatol,2016,175(Suppl 2):26-29. DOI:10.1111/bjd.14906.
[33] FANJUL-MOLES ML,LOPEZ-RIQUELME GO. Relationship between oxidative stress,circadian rhythms,and AMD[J]. Oxid Med Cell Longev,2016,2016:7420637. DOI:10.1155/2016/7420637.
[34] JARRETT SG,LEWIN AS,BOULTON ME. The importance of mitochondria in age-related and inherited eye disorders[J]. Ophthalmic Res,2010,44(3):179-190. DOI:10.1159/000316480.
[35] 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,2017,1863(1):21-32. DOI:10.1016/j.bbadis.2016.09.020.
[36] PENDERGRASS W,ZITNIK G,TSAI R,et al. X-ray induced cataract is preceded by LEC loss,and coincident with accumulation of cortical DNA,and ROS;similarities with age-related cataracts[J]. Mol Vis,2010,16:1496-1513.
[37] BABIZHAYEV MA,YEGOROV YE. Reactive Oxygen species and the aging eye:specific role of metabolically active mitochondria in maintaining lens function and in the initiation of the oxidation-induced maturity onset cataract-a novel platform of mitochondria-targeted antioxidants with broad therapeutic potential for redox regulation and detoxification of oxidants in eye diseases[J]. Am J Ther, 2016,23(1):e98-e117. DOI:10.1097/MJT.0b013e3181ea31ff.
[38] BABIZHAYEV MA. Mitochondria induce oxidative stress,generation of reactive oxygen species and redox state unbalance of the eye lens leading to human cataract formation:disruption of redox lens organization by phospholipid hydroperoxides as a common basis for cataract disease[J]. Cell Biochem Funct,2011,29(3):183-206. DOI:10.1002/cbf.1737.
[39] LEE S,VAN BERGEN NJ,KONG GY,et al. Mitochondrial dysfunction in glaucoma and emerging bioenergetic therapies[J]. Exp Eye Res,2011,93(2):204-212. DOI:10.1016/j.exer.2010.07.015.
[40] OSBORNE NN. Mitochondria:their role in ganglion cell death and survival in primary open angle glaucoma[J]. Exp Eye Res,2010,90(6):750-757. DOI:10.1016/j.exer.2010.03.008.
[41] JU WK,KIM KY,DUONG-POLK KX,et al. Increased optic atrophy type 1 expression protects retinal ganglion cells in a mouse model of glaucoma[J]. Mol Vis,2010,16:1331-1342.
[42] TANWAR M,DADA T,SIHOTA R,et al. Mitochondrial DNA analysis in primary congenital glaucoma[J]. Mol Vis,2010,16:518-533.
[43] KUMAR M,TANWAR M,FAIQ MA,et al. Mitochondrial DNA nucleotide changes in primary congenital glaucoma patients[J]. Mol Vis,2013,19:220-230.
[44] KIMURA A,NAMEKATA K,GUO X,et al. Targeting oxidative stress for treatment of glaucoma and optic neuritis[J]. Oxid Med Cell Longev,2017,2017:2817252. DOI:10.1155/2017/2817252.
[45] SANTOS JM,TEWARI S,LIN JY,et al. Interrelationship between activation of matrix metalloproteinases and mitochondrial dysfunction in the development of diabetic retinopathy[J]. Biochem Biophys Res Commun,2013,438(4):760-764. DOI:10.1016/j.bbrc.2013.07.066.
[46] MOHAMMAD G,KOWLURU RA. Matrix metalloproteinase-2 in the development of diabetic retinopathy and mitochondrial dysfunction[J]. Lab Invest,2010,90(9):1365-1372. DOI:10.1038/labinvest.2010.89.
[47] KOWLURU RA. Effect of reinstitution of good glycemic control on retinal oxidative stress and nitrative stress in diabetic rats[J]. Diabetes,2003,52(3):818-823.
[48] STITT AW,CURTIS TM. Advanced glycation and retinal pathology during diabetes[J]. Pharmacol Rep,2005,57(Suppl):156-168.
[49] GUSDON AM,VOTYAKOVA TV,MATHEWS CE. mt-Nd2a suppresses reactive oxygen species production by mitochondrial complexesⅠandⅢ[J]. J Biol Chem,2008,283(16):10690-10697. DOI:10.1074/jbc.M708801200.
[50] KENNEY MC,ATILANO SR,BOYER D,et al. Characterization of retinal and blood mitochondrial DNA from age-related macular degeneration patients[J]. Invest Ophthalmol Vis Sci,2010,51(8):4289-4297. DOI:10.1167/iovs.09-4778.
[51] DIB B,LIN H,MAIDANA DE,et al. Mitochondrial DNA has a pro-inflammatory role in AMD[J]. Biochim Biophys Acta,2015, 1853(11 Pt A):2897-2906. DOI:10.1016/j.bbamcr.2015.08.012.
[52] OLMO-AGUADO S,MANSO AG,OSBORNE NN. Light might directly affect retinal ganglion cell mitochondria to potentially influence function[J]. Photochem Photobiol,2012,88(6):1346-1355. DOI:10.1111/j.1751-1097.2012.01120.x.
[53] OSBORNE NN,KAMALDEN TA,MAJID AS,et al. Light effects on mitochondrial photosensitizers in relation to retinal degeneration[J]. Neurochem Res,2010,35(12):2027-2034. DOI:10.1007/s11064-010-0273-5.
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