[1]邓文政,邓平.MG53蛋白的研究进展[J].心血管病学进展,2015,(5):626-629.[doi:10.3969/j.issn.1004-3934.2015.05.027]
 DENG Wenzheng,DENG Ping.Research Progress of MG53[J].Advances in Cardiovascular Diseases,2015,(5):626-629.[doi:10.3969/j.issn.1004-3934.2015.05.027]
点击复制

MG53蛋白的研究进展()
分享到:

《心血管病学进展》[ISSN:51-1187/R/CN:1004-3934]

卷:
期数:
2015年5期
页码:
626-629
栏目:
综述
出版日期:
2016-05-20

文章信息/Info

Title:
Research Progress of MG53
作者:
邓文政1邓平2
1. 南华大学,湖南 衡阳 421001; 2. 长沙市中心医院心内科,湖南 长沙 410004
Author(s):
DENG Wenzheng1DENG Ping2
1. South of China,Hengyang 421001,Hunan,China; 2. Department of Cardiology,Changsha Central Hospital, Changsha 410004,Hunan,China
关键词:
冠心病 MG53蛋白 缺血前处理 缺血后处理 心肌细胞保护 胰岛素抵抗
Keywords:
coronary heart disease MG53 ischaemic preconditioning ischaemic postconditioning cardioprotection insulin resistance
分类号:
Q51; R541.4
DOI:
10.3969/j.issn.1004-3934.2015.05.027
文献标志码:
A
摘要:
近年来发现mitsugumin 53(MG53)蛋白是广泛表达于心肌和骨骼肌tripartite motif的家族成员之一。它可以通过与微囊蛋白-3结合后形成复合物进而与磷酸肌醇3-激酶的P85亚基结合激活再灌注损伤补救酶通路,借此参与缺血前处理和缺血后处理的心肌保护作用,减轻心肌缺血再灌注损伤。最新研究发现,MG53蛋白还可通过与胰岛素受体1结合后导致泛素依赖的胰岛素受体表达下降,最终导致胰岛素抵抗和代谢综合征。现介绍了MG53蛋白既有对心肌细胞的修复作用,与此同时,又会诱发胰岛素抵抗,这有望为冠心病和
Abstract:
In recent years, researchers have found that mitsugumin 53(MG53)is a relatively newly identified tripartite motif-containing family muscle-specific E3 ubiquitin ligase, which is expressed in both skeletal muscle and heart. The formation of a functional complex of MG53-CaV3-PI3K can activate the RISK way, thus MG53 plays acrucial role in IPC-mediated cardioprotection and post C-mediated cardioprotection. The new study found MG53 as E3 ligase targets the insulin receptor substrate 1 for degradation, therefore, has influence on insulin resistance and the metabolic syndrome. This paper introduces MG53's repair action on myocardial cells, while at the same time, can induce insulin resistance. This combination is expected to provide a new target for the treatment of coronary heart disease and metabolic syndrome.

参考文献/References:

[1] Weisleder N,Takizawa N,Lin P,et al.Recombinant MG53 protein modulates therapeutic cell membrane repair in treatment of muscular dystrophy[J].Sci Transl Med,2012,4(139):139ra85.
[2] He B,Tang RH,Weisleder N,et al.Enhancing muscle membrane repair by gene delivery of MG53 ameliorates muscular dystrophy and heart failure in delta-Sarcoglycan-deficient hamsters[J].Mol Ther,2012,20(4):727-735.
[3] 伊木清.MG53——肌细胞损伤的“分子绷带”[J].中国运动医学杂志,2012,12:1117-1121,1047.
[4] Penna C,Perrelli MG,Pagliaro P. Mitochondrial pathways,permeability transition pore,and redox signaling in cardioprotection:therapeutic implications [J].Antioxid Redox Signal,2013,18:556-599.
[5] Barrère-Lemaire S,Nargeot J,Piot C.Delayed postconditioning:not too late[J].Trends Cardiovasc Med,2012,22:173-179.
[6] Heusch G.Cardioprotection:chances and challenges of its translation to the clinic[J].Lancet,2013,381:166-175.
[7] Penna C,Perrelli MG,Pagliaro P.Mitochondrial pathways,permeability transition pore,and redox signaling in cardioprotection:therapeutic implications[J].Antioxid Redox Signal,2013,18:556-599.
[8] Murry CE,Jennings RB,Reimer KA.Preconditioning with ischemia:a delay of lethalcell injury in ischemic myocardium[J].Circulation,1986,74:1124-1136.
[9] Cao CM,Zhang Y,Weisleder N,et al.MG53 constitutes a primary determinant of cardiac ischemic preconditioning[J].Circulation,2010, 121(23):2565-2574.
[10] Wu QL,Shen T,Ma H.Sufentanil postconditioning protects the myocardium from ischemia-reperfusion via PI3K /Akt-GSK-3β pathway [J].J Surg Res,2012,178(2):563-570.
[11] Shiraishi I,Melendez J,Ahn Y, et al.Nuclear targeting of Akt enhances kinase activity and survival of cardiomyocytes[J].Circ Res,2004,94: 884-891.
[12] Howes AL,Arthur JF,Zhang T,et al.Akt-mediated cardiomyocyte survival pathways are compromised by G alpha q-induced phosphoinositide 4,5-bisphosphate depletion[J]. J Biol Chem,2003,278: 40343-40351.
[13] Tong H,Imahashi K,Steenbergen C,et al.Phosphorylation of glycogen synthase kinase-3beta during preconditioning through a phosphatidylinositol-3-kinase-dependent pathway is cardioprotective[J].Circ Res,2002,90:377-379.
[14] Chaudhary KR,Cho WJ,Yang F,et al.Effect of ischemia reperfusion injury and epoxyeicosatrienoic acids on caveolin expression mouse myocardium [J].J Cardiovasc Pharmacol,2013,61(3):258-263.
[15] 李静静,赵建力.窖蛋白与心血管系统疾病关系的研究进展[J]. 中西医结合心脑血管病杂志,2014,9:1124-1126.
[16] Cai C,Masumiya H,Weisleder N,et al.MG53 regulates membrane budding and exocytosis in muscle cells[J].J Biol Chem,2009,284: 3314-3322.
[17] Zhao H.Ischemic postconditioning as a novel avenue to protect against brain injury after stroke[J].J Cereb Blood Flow Metab,2009, 29(5):873-885.
[18] Zhang Y,Lv F,Jin L,et al.MG53 participates in ischaemic postconditioning through the RISK signalling pathway[J].Cardiovasc Res,2011,91(1):108-115.
[19] Lacerda L,Somers S,Opie LH,et al.Ischaemic postconditioning protects against reperfusion injury via the SAFE pathway[J].Cardiovasc Res,2009,84:201-208.
[20] Goodman MD,Koch SE,Fuller-Bicer GA,et al.Regulating RISK:a role for JAK-STAT signaling in postconditioning?[J].Am J Physiol Heart Circ Physiol,2008,295:H1649-H1656.
[21] 杜锦.代谢综合征研究进展[J].中华老年心脑血管病杂志,2015,4:447-448.
[22] Song R,Peng W,Zhang Y,et al.Central role of E3 ubiquitin ligase MG53 in insulin resistance and metabolic disorders[J].Nature, 2013,494(7437):375-379.
[23] Lee CS,Yi JS,Jung SY,et al.TRIM72 negatively regulates myogenesis via targeting insulin receptor substrate-1[J].Cell Death Differ,2010,17(8): 1254-1265.
[24] Hawkins K,Joy S, McKay T.Cell signalling pathways underlying induced pluripotent stem cell reprogramming[J].World J Stem Cells,2014,5:620-628.
[25] DeFronzo RA, Jacot E,Jequier E,et al.The effect of insulin on the disposal of intravenous glucose.Results from indirect calorimetry and hepatic and femoral venous catheterization[J].Diabetes,1981,30:1000-1007.
[26] Shulman GI,Rothman DL,Jue T,et al.Quantitation of muscle glycogen synthesis in normal subjects and subjects with non-insulin-dependent diabetes by 13C nuclear magnetic resonance spectroscopy[J].N Engl J Med,1990,322:223-228.
[27] Yi JS,Park JS,Ham YM,et al.MG53-induced IRS-1 ubiquitination negatively regulates skeletal myogenesis and insulin signaling[J].Nat Commun,2013,4:2354.doi:10.1038/ncomms3354.

相似文献/References:

[1]杜钧,佘强.冠心病抗炎治疗的临床研究进展[J].心血管病学进展,2016,(1):32.[doi:10.16806/j.cnki.issn.1004-3934.2016.01.009]
 DU Jun,SHE Qiang.Clinical Research Progress of Anti-inflammatory Therapy of Coronary Heart Disease[J].Advances in Cardiovascular Diseases,2016,(5):32.[doi:10.16806/j.cnki.issn.1004-3934.2016.01.009]
[2]努热曼古丽·阿布都克热木,马依彤.重度左心室收缩功能不全的冠心病患者血运重建治疗疗效及预后的评价[J].心血管病学进展,2016,(1):46.[doi:10.16806/j.cnki.issn.1004-3934.2016.01.012]
 NUREMANGULI·Abudukeremu,MA Yitong.Evaluation of Efficacy and Prognosis of Revascularization Therapy on Patients with Coronary Heart Disease and Severe Left Ventricular Systolic Dysfunction[J].Advances in Cardiovascular Diseases,2016,(5):46.[doi:10.16806/j.cnki.issn.1004-3934.2016.01.012]
[3]刘洋,综述,伍贵富,等.增强型体外反搏治疗冠心病的新机制[J].心血管病学进展,2016,(2):185.[doi:10.16806/j.cnki.issn.1004-3934.2016.02.023]
 LIU Yang,WU Guifu.New Mechanism of Enhanced External Counterpulsation for Treatment of Coronary Artery Disease[J].Advances in Cardiovascular Diseases,2016,(5):185.[doi:10.16806/j.cnki.issn.1004-3934.2016.02.023]
[4]杨洋,综述,沈比先,等.心脏核磁共振评估缺血性心脏病的应用价值[J].心血管病学进展,2016,(2):204.[doi:10.16806/j.cnki.issn.1004-3934.2016.02.028]
 YANG Yang,SHEN Bixian.Value of Cardiac Magnetic Resonance Assessment of Ischemic Heart Disease[J].Advances in Cardiovascular Diseases,2016,(5):204.[doi:10.16806/j.cnki.issn.1004-3934.2016.02.028]
[5]史敬,综述,马依彤,等.n-3多不饱和脂肪酸对心血管疾病的临床应用[J].心血管病学进展,2016,(3):278.[doi:10.16806/j.cnki.issn.1004-3934.2016.03.016]
 SHI Jing,MA Yitong.Effects of n-3 Polyunsaturated Fatty Acids on Cardiovascular Disease[J].Advances in Cardiovascular Diseases,2016,(5):278.[doi:10.16806/j.cnki.issn.1004-3934.2016.03.016]
[6]高柳,袁晋青.重复支架置入术治疗药物洗脱支架再狭窄的研究进展[J].心血管病学进展,2015,(5):555.[doi:10.3969/j.issn.1004-3934.2015.05.008]
 GAO Liu,YUAN Jingqing.Progress in Treatment for Drug-eluting Stent Restenosis by Re-implementation of Stents[J].Advances in Cardiovascular Diseases,2015,(5):555.[doi:10.3969/j.issn.1004-3934.2015.05.008]
[7]陈静,李兴德.冠心病患者服药依从性的研究进展[J].心血管病学进展,2015,(6):728.[doi:10.3969/j.issn.1004-3934.2015.06.018]
 CHEN Jing,LI Xingde.Advances in Medication Adherence of Patients with Coronary Heart Disease[J].Advances in Cardiovascular Diseases,2015,(5):728.[doi:10.3969/j.issn.1004-3934.2015.06.018]
[8]姚雯,毛露,孙硕,等.心源性外泌体作为冠心病标志物和新靶点展望[J].心血管病学进展,2019,(6):844.[doi:10.16806/j.cnki.issn.1004-3934.2019.06.002]
 YAO Wen,MAO Lu,SUN Shuo,et al.Exogenous Exosome as A New Marker and Target of Coronary Heart Disease[J].Advances in Cardiovascular Diseases,2019,(5):844.[doi:10.16806/j.cnki.issn.1004-3934.2019.06.002]
[9]郭彩艳 靳春荣.腺苷药物在心血管疾病诊治中的应用进展[J].心血管病学进展,2019,(7):1011.[doi:10.16806/j.cnki.issn.1004-3934.2019.07.012]
 GUO CaiyanJIN Chunrong.Progress in the Application of Adenosine Drugs in the Diagnosis and Treatment of Cardiovascular Diseases[J].Advances in Cardiovascular Diseases,2019,(5):1011.[doi:10.16806/j.cnki.issn.1004-3934.2019.07.012]
[10]方砚 王效浣 郭朝霞.血流介导性血管扩张评价心血管病患者肱动脉内皮功能的研究进展[J].心血管病学进展,2019,(5):793.[doi:10.16806/j.cnki.issn.1004-3934.2019.05.032]
 FANG Yan,WANG Xiaohuan,GUO Zhaoxia.Flow- mediated Vasodilation Evaluation of Brachial Artery Endothelial Function in Patients with Cardiovascular Disease[J].Advances in Cardiovascular Diseases,2019,(5):793.[doi:10.16806/j.cnki.issn.1004-3934.2019.05.032]

备注/Memo

备注/Memo:
作者简介:邓文政(1988—),住院医师,硕士,主要从事冠心病研究。Email: 407039925@qq.com 作者简介:邓平(1968—),主任医师,博士,主要从事心血管疾病研究。Email:1229015862@qq.com
更新日期/Last Update: 2016-05-20