期刊文献+

线粒体未折叠蛋白反应及其与神经系统疾病关系研究进展 被引量:2

下载PDF
导出
摘要 线粒体功能障碍,尤其是线粒体蛋白质稳态失衡,在许多人类疾病的发生发展中有重要作用。应激时发生的线粒体未折叠蛋白反应(mtUPR),通过分子伴侣和蛋白酶折叠降解有缺陷的蛋白质,维持线粒体蛋白稳态,保证细胞与机体健康。本文将从mtUPR的定义、激活、在线虫和哺乳动物身上的信号转导途径,以及mt UPR与神经系统疾病的关系予以综述,从而为尽早调节线粒体稳态平衡的干预目标提供新思路。
出处 《国际神经病学神经外科学杂志》 北大核心 2016年第4期362-366,共5页 Journal of International Neurology and Neurosurgery
基金 国家自然科学基金(81271414)
  • 相关文献

参考文献31

  • 1Kaushik S, Cuervo AM. Proteostasis and aging. Nat Med, 2015, 21(12) : 1406-1415.
  • 2Andreux PA, Houtkooper RH, Auwerx J. Pharmacological approaches to restore mitochondrial function. Nat Rev Drug Diseov, 2013, 12(6) : 465-483.
  • 3Jovaisaite V, Auwerx J. The mitochondrial unfolded protein response--synchronizing genomes. Curr Opin Cell Biol, 2015, 33: 74-81.
  • 4Zhao Q, Wang J, Levichkin IV, et al. A mitochondrial spe- cific stress response in mammalian cells. EMBO J, 2002, 21(17) : 4411-4419.
  • 5Yoneda T, Benedetti C, Urano F, et al. Compartment-spe- cific perturbation of protein handling activates genes encoding mitochondrial chaperones. J Cell Sci, 2004 , 117 ( 18 ) : 4055 -4066.
  • 6Owusu-Ansah E, Song W, Perrimon N. Muscle mitohormesis promotes longevity via systemic repression of insulin signaling. Cell, 2013, 155(3) : 699-712.
  • 7Houtkooper RH, Mouchiroud L, Ryu D, et al. Mitonuclear protein imbalance as a conserved longevity mechanism. Na- ture, 2013, 497(7450) : 451-457.
  • 8Kohler F, Muller-Rischart AK, Conradt B, et al. The loss of LRPPRC function induces the mitochondrial unfolded protein response. Aging (Albany NY) , 2015, 7(9) : 701.
  • 9Wu Y, Williams EG, Dubuis S, et al. Muhilayered genetic and omics dissection of mitochondrial activity in a mouse refer- ence population. Cell, 2014, 158(6) : 1415-1430.
  • 10Baker BM, Nargund AM, Sun T, et al. Protective coupling of mitochondrial function and protein synthesis via the eIF2 α kinase GCN-2. PLoS Genet, 2012, 8(6) : e1002760.

二级参考文献30

  • 1Bekris LM, Mata IF, Zabetian CP. The genetics of Parkinson disease. J C, eriatr Psychiatry Neurel, 2010, 23 ( 4 ) : 228 - 242.
  • 2Golpieh M, Rahmani B, Mohamed Ibrahim N, et al. Pre- conditioning as a Potential Strategy for the Prevention of Par- kinson' s Disease. Mol Neurebiol, 2014.
  • 3Exner N, Lutz AK, Haass C, et al. Mitochondrial dysfunc- tion in Parkinson ' s disease: molecular mechanisms and pathophysiological consequences. EMBO J, 2012, 31 (14) : 3038 -3062.
  • 4Ouazia D, Levros LC, JR Rassart E, et al. Dopamine down-regulation of protein L-isoaspartyl methyltransferase is dependent on reactive oxygen species in SH-SY5Y cells. Neuroscience, 2014, 267 (16) : 263-276.
  • 5Lin MT, Beal MF. Mitochondrial dysfunction and oxidative stress in neuredegenemtive diseases. Nature, 2006, 443 (7113) : 787-795.
  • 6Anand SK, Tikoo SK. Viruses as modulators of mitochondrial functions. Adv Virol, 2013, 2013: 738-794.
  • 7Rapaport D. Finding the right organelle. EMBO Rep, 2003, 4(10) : 948-952.
  • 8Sun YS, Lv LX, Zhao Z, et al. Cordycepol C Induces Caspase-Independent Apoptosis in Human Hepatocellular Car- cinoma HepG2 Cells. Biol Pharm Bull, 2014, 37 (4) : 608-617.
  • 9Cal T, Ottolini D, Brini M. Mitochondrial Ca (2 + ) and neurodegeneration. Cell Calcium, 2012 , 52 ( 1 ) : 73-85.
  • 10Gandhi S, Abramov AY. Mechanism of oxidative stress in neurodegeneration. Oxid Med Cell Longev, 2012, 2012: 428010.

共引文献9

同被引文献20

引证文献2

二级引证文献13

相关作者

内容加载中请稍等...

相关机构

内容加载中请稍等...

相关主题

内容加载中请稍等...

浏览历史

内容加载中请稍等...
;
使用帮助 返回顶部