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泛素-蛋白酶体系统在心肌梗死中的病理生理意义 被引量：3

Pathophysiological significance of ubiquition-proteasome system in myocardial infarction
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摘要 Degradation of most proteins in eukaryotic cells is through the ubiquition-proteasome system(UPS).Recently,it demonstrated that UPS regulates cell apoptosis and cardiac hypertrophy.The differences of UPS regulation lie in E3 ligases,which specifically recognize targets and direct the ubiquitination process.Recent evidence suggests that atrogin-1/muscle atrophy F-box(Mafbx) and muscle RING finger 1(MuRF1) may be critical mediators of the heart and muscle atrophy and hypertrophy.This review summarizes the possible relationship between UPS and cardiac dysfunction after myocardial infarction in order to inhibit cardiac dysfunction after myocardial infarction. Degradation of most proteins in eukaryotic cells is through the ubiquition - proteasome system （UPS）. Recently, it demonstrated that UPS regulates cell apoptosis and cardiac hypertrophy. The differences of UPS regulation lie in E3 ligases, which specifically recognize targets and direct the ubiquitination process. Recent evidence suggests that atrogin - 1/muscle atrophy F - box （Mafbx） and muscle RING finger 1 （ MuRF1 ） may be critical mediators of the heart and muscle atrophy and hypertrophy. This review summarizes the possible relationship between UPS and cardiac dysfunction after myocardial infarction in order to inhibit cardiac dysfunction after myocardial infarction.
作者 张赟 戴翠莲
机构地区 合肥医学院附属医院心内科
出处 《中国病理生理杂志》 CAS CSCD 北大核心 2010年第6期1234-1236,1243,共4页 Chinese Journal of Pathophysiology
基金 国家自然科学基金资助项目(No.30860295)
关键词 泛素-蛋白酶体系统 心脏 心肌梗死 Ubiquitin proteasome system Heart Myocardial infarction
分类号 R543 [医药卫生—心血管疾病]
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参考文献21

  • 1Herrmann J,Ciechanover A,Lerman LO,et al.The ubiquitin-proteasome system in cardiovascular diseases-a hypothesis extended[J].Cardiovasc Res,2004,61(1):11-21.
  • 2Willis MS,Patterson C.Into the heart:the emerging role of the ubiquitin-proteasome system[J].J Mol Cell Cardiol,2006,41(4):567-579.
  • 3Wang X,Robbins J.Heart failure and protein quality control[J].Circ Res,2006,99 (12):1315-1328.
  • 4Tsukamoto O,Minamino T,Okada K,et al.Depression of proteasome activities during the progression of cardiac dysfunction in pressure-overloaded heart of mice[J].Biochem Biophys Res,2006,340(4):1125-1133.
  • 5戴翠莲,罗开良.泛素-蛋白酶体系统与动脉粥样硬化性疾病的发生[J].国际心血管病杂志,2006,33(3):169-172. 被引量：3
  • 6Fielitz J,van Rooij E,Spencer JA,et al.Loss of muscle-specific RING-finger 3 predisposes the heart to cardiac rupture after myocardial infarction[J].Proc Natl Acad Sci USA,2007,104(11):4377-4382.
  • 7Li HH,Willis MS,Lockyer P,et al.Atrogin-1 inhibits Akt-dependent cardiac hypertrophy in mice via ubiquitin-dependent coactivation of Forkhead proteins[J].J Clin Invest,2007,117(11):3211-3223.
  • 8Sandri M,Sandri C,Gilbert A,et al.Foxo transcription factors induce the atrophy-related ubiquitin ligase atrogin-1 and cause skeletal muscle atrophy[J].Cell,2004,117(3):399-412.
  • 9Gomes MD,Lecker SH,Jagoe RT,et al.Atrogin-1,a muscle-specific F-box protein highly expressed during muscle atrophy[J].Proc Natl Acad Sci USA,2001,98(25):14440-14445.
  • 10Baines CP,Molkentin JD.STRESS signaling pathways that modulate cardiac myocyte apoptosis[J].J Mol Cell Cardiol,2005,38(1):47-62.

二级参考文献16

  • 1[1]Ciechanover A,Orian A,Schwartz AL.The ubiquitin-mediated proteolytic pathway:mode of action and clinical implication[J].Cell Biochem,Suppl,2000;77(S34):40-51.
  • 2[2]Li Q,Verma IM.NF-B regulation in the immune system[J].Nat Rev Immunol,2002,2(10):725-734.
  • 3[3]Inoue T,Geyer RK,Howard D,Yu ZK,Maki GG.MDM2can promote the ubiquitination,nuclear export,and degradation of p53 in the absence of direct binding[J].Biol Chem,2001,276(48):45255-45260
  • 4[4]Bornstein G,Bloom J,Sitry-Shevah D,et al.Role of the SCFSkp2 ubiquitin ligase in the degradation of p21 Cip1 in S phase[J].Biol Chem,2003,278 (28):25752-25757.
  • 5[5]Canty TG Jr,Boyle EM Jr,Farr A.et al.Oxidative stress induces NF-kappa B nuclear translocation without degradation of IkappaB-alpha[J].Circulation,1999,100(19 Suppl):Ⅱ361-Ⅱ364.
  • 6[6]Stangl V,Lorenz M,Meiners S,et al.Long-term up-regulation of eNOS and improvement of endothelial function by inhibition of the ubiquitin-proteasome pathway[J].FASEBJ,2004,18(2):272-279.
  • 7[7]Esteban,Ruperez M,Sanchez-Lopez,et al.Angiotensin Ⅳactivates the nuclear transcription factor-kappa B and related proinflammatory genes in vascular smooth muscle cells[J].Circulation Research,2005,96(9):965-973.
  • 8[8]Hermann J,Gulati R,Napoli C,et al.Oxidative stress-related increase in ubiquitination in early coronary atherosclerosis[J].FASEB,2003,17(12):1730-1732.
  • 9[9]Thyberg J,Blomgren K.Effects of proteasome and calpain inhibitors on the structural reorganization and proliferation of vascular smooth muscle cells in primary culture[J].Lab Invest,1999,79(9):1077-1088.
  • 10[10]Meiners S,Laule M,Rother W,et al.Ubiquitin proteasome pathway as a new target for the prevention of restenosis[J].Circulation,2002,105(4):483-489.

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中国病理生理杂志
2010年 第6期

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