[1]张媛媛,李筱荣,邵彦.糖尿病视网膜病变“代谢记忆”与线粒体功能相关性研究进展[J].眼科新进展,2023,43(12):1005-1008.[doi:10.13389/j.cnki.rao.2023.0200]
 ZHANG Yuanyuan,LI Xiaorong,SHAO Yan.Research progress on the correlation between metabolic memory and mitochondrial function in diabetic retinopathy[J].Recent Advances in Ophthalmology,2023,43(12):1005-1008.[doi:10.13389/j.cnki.rao.2023.0200]
点击复制

糖尿病视网膜病变“代谢记忆”与线粒体功能相关性研究进展/HTML
分享到:

《眼科新进展》[ISSN:1003-5141/CN:41-1105/R]

卷:
43卷
期数:
2023年12期
页码:
1005-1008
栏目:
文献综述
出版日期:
2023-12-05

文章信息/Info

Title:
Research progress on the correlation between metabolic memory and mitochondrial function in diabetic retinopathy
作者:
张媛媛李筱荣邵彦
300384 天津市,天津医科大学眼科医院、眼视光学院、眼科研究所,国家眼耳鼻喉疾病临床医学研究中心天津市分中心,天津市视网膜功能与疾病重点实验室
Author(s):
ZHANG YuanyuanLI XiaorongSHAO Yan
Tianjin Key Laboratory of Retinal Functions and Diseases,Tianjin Branch of National Clinical Research Center for Ocular Disease,Eye Institute and School of Optometry,Tianjin Medical University Eye Hospital,Tianjin 300384,China
关键词:
线粒体代谢记忆糖尿病视网膜病变氧化应激糖尿病
Keywords:
mitochondria metabolic memory diabetic retinopathy oxidative stress diabetes
分类号:
R774.1
DOI:
10.13389/j.cnki.rao.2023.0200
文献标志码:
A
摘要:
糖尿病视网膜病变(DR)是由糖尿病导致的严重致盲性眼病。多项研究表明糖尿病患者体内存在“代谢记忆”现象,但其相关机制目前尚不清楚。在DR的发病和进展过程中,高血糖环境下氧化应激使DR患者视网膜细胞中线粒体DNA(mtDNA)拷贝数异常发生突变,其修复系统同时遭到破坏并形成恶性循环,造成体内活性氧(ROS)过量生成、氧化还原稳态破坏和细胞凋亡等现象发生。由于mtDNA可以进行独立复制并遗传给下一代,同时表观遗传学修饰也会影响与DR发病机制相关基因的调节。在DR发生发展过程中,明确线粒体损伤和“代谢记忆”现象的发生机制对DR的预防和治疗具有重要意义,线粒体转移技术的出现将有望打破“代谢记忆”现象,为此类疾病的治疗开辟新的途径。本文就其相关研究及发展做一综述。
Abstract:
Diabetic retinopathy (DR) is a severe blinding eye disease caused by diabetes. A number of studies have shown that there is a phenomenon of “metabolic memory” in diabetic patients, but its mechanism is still unclear. In the occurrence and progression of DR, oxidative stress in a high-glucose environment causes abnormal mutations of mitochondrial DNA (mtDNA) copy number in retinal cells, and its repair system is destroyed at the same time and forms a vicious circle, resulting in excessive production of reactive oxygen, destruction of redox homeostasis and apoptosis. The mtDNA can be independently replicated and passed on to the next generation, and epigenetic modification can also affect the regulation of genes related to the pathogenesis of DR. In the occurrence and development of DR, it is of great significance to clarify the mechanism of mitochondrial damage and “metabolic memory” for the prevention and treatment of DR. The emergence of mitochondrial transfer technology is expected to break the “metabolic memory” phenomenon and open up new avenues for treating such diseases. This article gives a review of the related research and development.

参考文献/References:

[1] REDDY M A,ZHANG E,NATARAJAN R.Epigenetic mechanisms in diabetic complications and metabolic memory[J].Diabetologia,2015,58(3):443-455.
[2] SUN H,SAEEDI P,KARURANGA S,PINKEPANK M,OGURTSOVA K,DUNCAN B B,et al.IDF diabetes atlas:global,regional and country-level diabetes prevalence estimates for 2021 and projections for 2045[J].Diabetes Res Clin Pract,2022,183:109119.
[3] ENGERMAN R L,KERN T S.Progression of incipient diabetic retinopathy during good glycemic control[J].Diabetes,1987,36(7):808-812.
[4] ANTONETTI D A,SILVA P S,STITT A W.Current understanding of the molecular and cellular pathology of diabetic retinopathy[J].Nat Rev Endocrinol,2021,17(4):195-206.
[5] NATHAN D M.Realising the long-term promise of insulin therapy:the DCCT/EDIC study[J].Diabetologia,2021,64(5):1049-1058.
[6] ZHANG L W,CHEN B H,TANG L S.Metabolic memory:mechanisms and implications for diabetic retinopathy[J].Diabetes Res Clin Pract,2012,96(3):286-293.
[7] NATHAN D M,CLEARY P A,BACKLUND J Y,GENUTH S M,LACHIN J M,ORCHARD T J,et al.Intensive diabetes treatment and cardiovascular disease in patients with type 1 diabetes[J].N Engl J Med,2005,353(25):2643-2653.
[8] Writing Team for the Diabetes Control and Complications Trial/Epidemiology of Diabetes Interventions and Complications Research Group.Effect of intensive therapy on the microvascular complications of type 1 diabetes mellitus[J].JAMA,2002,287(19):2563-2569.
[9] Writing Team for the Diabetes Control and Complications Trial/Epidemiology of Diabetes Interventions and Complications Research Group.Sustained effect of intensive treatment of type 1 diabetes mellitus on development and progression of diabetic nephropathy:the Epidemiology of Diabetes Interventions and Complications (EDIC) Study[J].JAMA,2003,290(16):2159-2167.
[10] LACHIN J M,GENUTH S,CLEARY P,DAVIS M D,NATHAN D M.Retinopathy and nephropathy in patients with type 1 diabetes four years after a trial of intensive therapy[J].N Engl J Med,2000,342(6):381-389.
[11] TSUBOI T,LEFF J,ZID B M.Post-transcriptional control of mitochondrial protein composition in changing environmental conditions[J].Biochem Soc Trans,2020,48(6):2565-2578.
[12] SHAMEKHI AMIRI F.Intracellular organelles in health and kidney disease[J].Nephrol Ther,2019,15(1):9-21.
[13] SCIAL F,SRIRAM A,STEFANATOS R,SPRIGGS R V,LOH S H Y,MARTINS L M,et al.Mitochondrial complex I derived ROS regulate stress adaptation in drosophila melanogaster[J].Redox Biol,2020,32:101450.
[14] KANG H Y,MA X J,LIU J J,FAN Y B,DENG X Y.High glucose-induced endothelial progenitor cell dysfunction[J].Diab Vasc Dis Res,2017,14(5):381-394.
[15] WU Y,SUN L K,ZHUANG Z D,HU X Q,DONG D L.Mitochondrial-derived peptides in diabetes and its complications[J].Front Endocrinol(Lausanne),2021,12:808120.
[16] DEHGHAN M,GHORBANI F,NAJAFI S,RAVAEI N,KARIMIAN M,KALHOR K,et al.Progress toward molecular therapy for diabetes mellitus:a focus on targeting inflammatory factors.[J].Diabetes Res Clin Pract,2022,189:109945.
[17] BROWNLEE M.Biochemistry and molecular cell biology of diabetic complications[J].Nature,2001,414(6865):813-820.
[18] ZENG Z,YUAN Q,YU R,ZHANG J,MA H,CHEN S.Ameliorative effects of probiotic lactobacillus paracasei NL41 on insulin sensitivity,oxidative stress,and beta-cell function in a type 2 diabetes mellitus rat model[J].Mol Nutr Food Res,2019,63(22):e1900457.
[19] WU M Y,YIANG G T,LAI T T,LI C J.The oxidative stress and mitochondrial dysfunction during the pathogenesis of diabetic retinopathy[J].Oxid Med Cell Longev,2018,2018:3420187.
[20] LI X,JIN Y L.Inhibition of miR-182-5p attenuates ROS and protects against myocardial ischemia-reperfusion injury by targeting STK17A[J].Cell Cycle,2022,1:1-12.
[21] ALBASHER G,ALKAHTANI S,AL-HARBI L N.Urolithin a prevents streptozotocin-induced diabetic cardiomyopathy in rats by activating SIRT1[J].Saudi J Biol Sci,2022,29(2):1210-1220.
[22] BERNEBURG M,KAMENISCH Y,KRUTMANN J.Repair of mitochondrial DNA in aging and carcinogenesis[J].Photochem Photobiol Sci,2006,5(2):190-198.
[23] VAYALIL P K.Mitochondrial oncobioenergetics of prostate tumorigenesis[J].Oncol Lett,2019,18(5):4367-4376.
[24] WALLACE D C.Mitochondrial genetic medicine[J].Nat Genet,2018,50(12):1642-1649.
[25] BRSER C,KELLER-FINDEISEN J,JAKOBS S.The TFAM-to-mtDNA ratio defines inner-cellular nucleoid populations with distinct activity levels[J].Cell Rep,2021,37(8):110000.
[26] GUSTAFSON M A,SULLIVAN E D,COPELAND W C.Consequences of compromised mitochondrial genome integrity[J].DNA Repair (Amst),2020,93:102916.
[27] MOHAMMAD G,KOWLURU R A.Mitochondrial dynamics in the metabolic memory of diabetic retinopathy[J].J Diabetes Res,2022,2022:3555889.
[28] KOWLURU R A,MOHAMMAD G.Epigenetics and mitochondrial stability in the metabolic memory phenomenon associated with continued progression of diabetic retinopathy[J].Sci Rep,2020,10(1):6655.
[29] CEN X F,ZHANG M K,ZHOU M X,YE L Z,XIA H G.Mitophagy regulates neurodegenerative diseases[J].Cells,2021,10(8):1876.
[30] PROVASEK V E,MITRA J,MALOJIRAO V H,HEGDE M L.DNA double-strand breaks as pathogenic lesions in neurological disorders[J].Int J Mol Sci,2022,23(9):4653.
[31] LINNANE A W,MARZUKI S,OZAWA T,TANAKA M.Mitochondrial DNA mutations as an important contributor to ageing and degenerative diseases[J].Lancet,1989,1(8639):642-645.
[32] SCARPULLA R C.Transcriptional paradigms in mammalian mitochondrial biogenesis and function[J].Physiol Rev,2008,88(2):611-638.
[33] JIANG M,XIE X,ZHU X F,JIANG S,MILENKOVIC D,MISIC J,et al.The mitochondrial single-stranded DNA binding protein is essential for initiation of mtDNA replication[J].Sci Adv,2021,7(27).
[34] MALIK A N,ROSA H S,DE MENEZES E S,TAMANG P,HAMID Z,NAIK A,et al.The detection and partial localisation of heteroplasmic mutations in the mitochondrial genome of patients with diabetic retinopathy[J].Int J Mol Sci,2019,20(24).
[35] MILLER D J,CASCIO M A,ROSCA M G.Diabetic retinopathy:The role of mitochondria in the neural retina and microvascular disease[J].Antioxidants (Basel),2020,9(10):905.
[36] SALLMYR A,RASHID I,BHANDARI S K,NAILA T,TOMKINSON AE.Human DNA ligases in replication and repair[J].DNA Repair (Amst),2020,93:102908.
[37] DURAISAMY A J,MOHAMMAD G,KOWLURU R A.Mitochondrial fusion and maintenance of mitochondrial homeostasis in diabetic retinopathy[J].Biochim Biophys Acta Mol Basis Dis,2019,1865(6):1617-1626.
[38] KOWLURU R A,SHAN Y.Role of oxidative stress in epigenetic modification of MMP-9 promoter in the development of diabetic retinopathy[J].Graefes Arch Clin Exp Ophthalmol,2017,255(5):955-962.
[39] MASSER D R,OTALORA L,CLARK N W,KINTER M T,ELLIOTT M H,FREEMAN W M.Functional changes in the neural retina occur in the absence of mitochondrial dysfunction in a rodent model of diabetic retinopathy[J].J Neurochem,2017,143(5):595-608.
[40] BORDONI L,PERUGINI J,PETRACCI I,MERCURIO E D,LEZOCHE G,GUERRIERI M,et al.Mitochondrial DNA in visceral adipose tissue in severe obesity:from copy number to D-Loop methylation[J].Front Biosci (Landmark Ed),2022,27(6):172.
[41] NOLFI-DONEGAN D,BRAGANZA A,SHIVA S.Mitochondrial electron transport chain:oidative phosphorylation,oxidant production,and methods of measurement[J].Redox Biol,2020,37:101674.
[42] KOWLURU R A.Retinopathy in a diet-induced type 2 diabetic rat model and role of epigenetic modifications[J].Diabetes,2020,69(4):689-698.
[43] MISHRA M,KOWLURU R A.Epigenetic modification of mitochondrial DNA in the development of diabetic retinopathy[J].Invest Ophthalmol Vis Sci,2015,56(9):5133-5142.
[44] YOSHINAGA A,KAJIHARA N,KUKIDOME D,MOTOSHIMA H,MATSUMURA T,NISHIKAWA T,et al.Hypoglycemia induces mitochondrial reactive oxygen species production through increased fatty acid oxidation and promotes retinal vascular permeability in diabetic mice[J].Antioxid Redox Signal,2021,34(16):1245-1259.
[45] MAGAGNOTTI C,ZERBINI G,FERMO I,CARLETTI R M,BONFANTI R,VALLONE F,et al.Identification of nephropathy predictors in urine from children with a recent diagnosis of type 1 diabetes[J].J Proteomics,2019,193:205-216.
[46] YIN L,ZHANG T,WEI Y,CAI W J,FENG G,CHANG X Y,et al.Epigenetic regulation of microRNA-375 and its role as DNA epigenetic marker of type 2 diabetes mellitus in Chinese Han population[J].Int J Clin Exp Pathol,2017,10(12):11986-11994.
[47] CHAKRABORTY A,VISWANATHAN P.Methylation-demethylation dynamics:implications of changes in acute kidney injury[J].Anal Cell Pathol (Amst),2018,2018:8764384.
[48] MISHRA M,KOWLURU R A.DNA methylation-a potential source of mitochondria DNA base mismatch in the development of diabetic retinopathy[J].Mol Neurobiol,2019,56(1):88-101.
[49] KATO M,NATARAJAN R.Epigenetics and epigenomics in diabetic kidney disease and metabolic memory[J].Nat Rev Nephrol,2019,15(6):327-345.
[50] CHEN K,LU P,BEERAKA N M,SUKOCHEVA O A,MADHUNAPANTULA S V,LIU J,et al.Mitochondrial mutations and mitoepigenetics:focus on regulation of oxidative stress-induced responses in breast cancers[J].Semin Cancer Biol,2022,83:556-569.

相似文献/References:

[1]刘海萍,辛晓蓉.黄芪复方对急性低压低氧大鼠视网膜线粒体损伤的保护作用[J].眼科新进展,2020,40(2):110.[doi:10.13389/j.cnki.rao.2020.0027]
 LIU Haiping,XIN Xiaorong.Protective effect of Radix Astragali seu Hedysari Compound on retinal mitochondrion injury caused by acute hypobaric hypoxia in rats[J].Recent Advances in Ophthalmology,2020,40(12):110.[doi:10.13389/j.cnki.rao.2020.0027]
[2]何美芹,韩国鸽,危平辉.线粒体相关内质网膜在年龄相关性黄斑变性发病机制中的作用研究进展[J].眼科新进展,2020,40(8):780.[doi:10.13389/j.cnki.rao.2020.0178]
 HE Meiqin,HAN Guoge,WEI Pinghui.Progress on mitochondrial-associated endoplasmic reticulum membranes in the pathogenesis of age-related macular degeneration[J].Recent Advances in Ophthalmology,2020,40(12):780.[doi:10.13389/j.cnki.rao.2020.0178]
[3]黎昌江,李秋慧,洪娟,等.黄芪甲苷对蓝光诱导损伤的视网膜色素上皮细胞的保护作用及其机制[J].眼科新进展,2021,41(11):1006.[doi:10.13389/j.cnki.rao.2021.0212]
 LI Changjiang,LI Qiuhui,HONG Juan,et al.Protective effect of Astragaloside IV on the blue light-induced damage of retinal pigment epithelium and its mechanism[J].Recent Advances in Ophthalmology,2021,41(12):1006.[doi:10.13389/j.cnki.rao.2021.0212]
[4]温艳君,张雪蕊,韦严,等.高糖环境下Ndufa4线粒体复合体相关蛋白2(Ndufa4l2)对小鼠视网膜感光细胞661W的影响[J].眼科新进展,2022,42(4):262.[doi:10.13389/j.cnki.rao.2022.0053]
 WEN Yanjun,ZHANG Xuerui,WEI Yan,et al.Effects of Ndufa4 mitochondrial complex associated like 2 on 661W cells exposed to high glucose[J].Recent Advances in Ophthalmology,2022,42(12):262.[doi:10.13389/j.cnki.rao.2022.0053]
[5]王紫郦,魏婷婷,谢田华,等.线粒体功能紊乱在糖尿病视网膜病变中作用的研究进展[J].眼科新进展,2022,42(12):999.[doi:10.13389/j.cnki.rao.2022.0204]
 WANG Zili,WEI Tingting,XIE Tianhua,et al.Research progress on the role of mitochondrial dysfunction in diabetic retinopathy[J].Recent Advances in Ophthalmology,2022,42(12):999.[doi:10.13389/j.cnki.rao.2022.0204]
[6]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.[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(12):238.[doi:10.13389/j.cnki.rao.2023.0049]
[7]蔡梦霞,魏婷婷,朱凌鹏,等.细胞衰老在干性年龄相关性黄斑变性中的作用研究进展[J].眼科新进展,2024,44(4):324.[doi:10.13389/j.cnki.rao.2024.0063]
 CAI Mengxia,WEI Tingting,ZHU Lingpeng,et al.Research progress on the role of cell aging in dry age-related macular degeneration[J].Recent Advances in Ophthalmology,2024,44(12):324.[doi:10.13389/j.cnki.rao.2024.0063]

备注/Memo

备注/Memo:
国家自然科学基金资助(编号:81900891)
更新日期/Last Update: 2023-12-05