期刊文献+

线粒体通透性转换孔与心肌缺血再灌注损伤

Mitochondrial permeability transition pore and myocardial ischemia-reperfusion injury
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摘要 线粒体通透性转换孔(mitochondrialpermeabilitytransitionpore,MPTP)是位于线粒体内、外膜之间的非特异性孔道,是由多种线粒体蛋白构成的复合体。目前,国内外研究已经证实,MPTP开放所引起的线粒体通透性变化在细胞凋亡过程中发挥了重要作用。随着研究的深入,人们发现缺血、缺氧、氧化应激等刺激因素都可能引起MPTP开放,使线粒体通透性发生改变,从而对多种疾病的发生、发展过程产生影响。本文就MPTP及其与心肌缺血再灌注损伤的关系进展情况作一综述。
作者 杨新征 于飞
机构地区 解放军第 解放军第
出处 《局解手术学杂志》 2015年第6期668-670,共3页 Journal of Regional Anatomy and Operative Surgery
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参考文献25

  • 1Elrod JW, Molkeutin JD. Physiologic functions of cyclophilin D and the mitochondrial permeability transition pore [ J ]. Cire J, 2013,77 ( 5 ) : 1111 - 1122.
  • 2雷艳,董兆君.环孢素A对大鼠缺血缺氧后酸碱平衡的调节作用[J].局解手术学杂志,2013,22(4):374-376. 被引量:4
  • 3Vaseva AV, Marchenko ND, Ji K, et al. p53 opens the mitochondrial per- meability transition pore to trigger necrosis [ J l. Ce11,2012, 149 (7): 1536 - 1548.
  • 4Vogelpohl I, Vetter R, Heger J,et al. Transgenic overexpression of heart- specific adenine nueleotide translocase 1 positively affects contractile function in cardiomyocytes [ J ]. Cell Physiol Biochem, 2011,27 ( 2 ) : 121 - 128.
  • 5Yarana C,Sripetchwandee J, Sanit J, et al. Calcium-induced cardiac mi- tochondrial dysfunction is predominantly mediated by cyclosporine A-de- pendent mitochondrial permeability transition pore [ J ]. Arch Med Res, 2012,43(5) :333 -338.
  • 6Tsujimoto Y, Nakagawa T, Shimizu S. Mitochondrial membrane permea- bility transition and cell death [ J ]. Biochim Biophys Acta, 2006, 1757(9 - 10) :1297 - 1300.
  • 7Joo HK, Lee YR, Lim SY, et al. Peripheral benzodiazepine receptor regu- lates vascular endothelial activations via suppression of the voltage-de- pendent anion channel-1 [ J ]. FEBS Lett ,2012,586 ( 9 ) : 1349 - 1355.
  • 8De Giorgi M, Voisin Chiret AS, Rault S. Targeting the BH3 domain of Bel-2 family proteins. A brief history from natural products to foldamers as promising cancer therapeutic avenues : J 1. Curr Med Chem, 2013, 20(24) :2964 -2978.
  • 9Shalbueva N, Mareninova OA, Gerloff A, et al. Effects of oxidative alcohol metabolism on the mitochondrial permeability transition pore and necrosisin a mouse model of alcoholic pancreatitis [ J ]. Gastroenterology, 2013, 144(2) :437 -446.
  • 10Pereira C, Silva RD, Saraiva L, et al. Mitochondria-dependent apoptosis in yeast[ J ]. Biochim Biophys Acta Bioenerg,2008,1783 (7) : 1286 - 1302.

二级参考文献22

  • 1Maria-Giulia Perrelli,Pasquale Pagliaro,Claudia Penna.Ischemia/reperfusion injury and cardioprotective mechanisms:Role of mitochondria and reactive oxygen species[J].World Journal of Cardiology,2011,3(6):186-200. 被引量:64
  • 2谢晓阳,李朝先,向小勇.心脏不停跳手术患者心肌线粒体变化的观察[J].中国胸心血管外科临床杂志,2005,12(1):66-67. 被引量:8
  • 3李世康,何巍,李逢昌,周华富,黄健辉,陈存荣.逆行灌注心脏不停跳双瓣膜置换术围术期心肌细胞凋亡及Bcl-2,Bax的表达[J].中国胸心血管外科临床杂志,2006,13(5):360-361. 被引量:5
  • 4Zomv DB, Juhaszova M, Yaniv Y, et al. Regulation and pharmacology of the mitochondrial permeability transition pore [ J ]. Cardiovasc Res, 2009,83(2) :213 -225.
  • 5Gomez L,Paillard M,Thibault H,et al. Inhibition of GSK3beta by post- conditioning is required to prevent opening of the mitochondrial permea- bility transition pore during reperfusion [ J ]. Circulation, 2008, 117 (21) :2761 -2768.
  • 6Joza N, Susin SA, Daugas E, et al. Essential role of the mitoehondrial apoptosis-inducing factor in progranuned cell death [ J ]. Nature, 2001, 410 (6828) :549 - 554.
  • 7Borutaite V, Brown GC. Mitochondria in apoptosis of ischemic heart [J]. FEBS Lett,2003,541 (1 -3) :1 -5.
  • 8ONG S B, SUBRAYAN S, LIM S Y, et al. Inhibiting mitochondrial fission protects the heart against ischemia/reperfusion injury [J]. Circulation, 2010, 121(18): 2012-2022.
  • 9HEUSCH G, BOENGLER K, SCHULZ R, et al. Cardioprotection: nitricoxide, protein kinases, and mitochondria[J]. Circulation, 2008, 118(19): 1915-1919.
  • 10HALESTRAP A P. Mitochondria and reperfusion injury of the heart- A holey death but not beyond salvation[J]. J Bioenerg Biomembr, 2009, 41 ( 2 ) : 113 - 121.

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