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细胞程序性死亡与心肌再灌注损伤的研究进展 被引量:8

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摘要 心肌梗死、心力衰竭等心血管疾病发展过程涉及多种细胞死亡形式,包括坏死、凋亡及自噬等。既往认为坏死是被动的不受信号转导调控的过程,而目前研究认为至少有一部分坏死是受信号调节的,程序性坏死是一种依赖于受体相互作用蛋白激酶(RIPK)3的细胞死亡,这种死亡过程由特定的信号转导分子所驱动,其特点是形成以RIPK1和RIPK3为核心的坏死小体。
作者 刘丽凤 王禹
出处 《中华老年心脑血管病杂志》 CAS 2015年第5期549-550,共2页 Chinese Journal of Geriatric Heart,Brain and Vessel Diseases
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  • 1Rafiq K,Kolpakov MA,Seqqat R,et al.c-Cbl inhibition improves cardiac function and survival in response to myocardial ischemia.Circulation,2014,129:2031-2043.
  • 2Chavez-Valdez R,Martin LJ,Flock DL,et al.Necrostatin-1attenuates mitochondrial dysfunction in neurons and astrocytes following neonatal hypoxia-ischemia.Neuroscience,2012,219:192-203.
  • 3Li L,Chen Y,Doan J,et al.Transforming growth factorβ-activated kinase 1signaling pathway critically regulates myocardial survival and remodeling.Circulation,2014,130:2162-2172.
  • 4Lukens JR,Vogel P,Johnson GR,et al.RIP1-driven autoinflammation targets IL-1αindependently of inflammasomes and RIP3.Nature,2013,498:224-227.
  • 5Lin J,Li H,Yang M,et al.A role of RIP3-mediated macrophage necrosis in atherosclerosis development.Cell Rep,2013,3:200-210.
  • 6Oberst A,Dillon CP,Weinlich R,et al.Catalytic activity of the caspase-8-FLIP(L)complex inhibits RIPK3-dependent necrosis.Nature,2011,471:363-367.
  • 7O'Donnell MA,Perez-Jimenez E,Oberst A,et al.Caspase 8inhibits programmed necrosis by processing CYLD.Nat Cell Biol,2011,13:1437-1442.
  • 8Ofengeim D,Yuan J.Regulation of RIP1kinase signalling at the crossroads of inflammation and cell death.Nat Rev Mol Cell Biol,2013,14:727-736.
  • 9Li J,McQuade T,Siemer AB,et al.The RIP1/RIP3necrosome forms a functional amyloid signaling complex required for programmed necrosis.Cell,2012,150:339-350.
  • 10Degterev A,Hitomi J,Germscheid M,et al.Identification of RIP1kinase as a specific cellular target of necrostatins.Nat Chem Biol,2008,4:313-321.

同被引文献61

  • 1潘伟,贾俊海.缺血预处理对糖尿病大鼠心肌缺血再灌注损伤的影响[J].中国全科医学,2009,12(8):649-650. 被引量:7
  • 2田锐,秦仁义,杜志勇,夏维.肿瘤坏死因子相关凋亡诱导配体的抗胰腺癌细胞的作用[J].中国普通外科杂志,2006,15(11):821-825. 被引量:5
  • 3Stadnik M, Handzlik-Orlik G, Sarnecki K. Clinical aspects of the use of trimetazidine in the prevention and treatment of myocardial diseases[J].Przegl Lek, 2013,70(9) : 730-734.
  • 4Bu]a LM. Myocardial ischemia and reper~usion iniury [J].Cardiovasc Pathol, 2005,14 (4) .. 170-175.
  • 5Ong SB, Samangouei P, Kalkhoran SB, et al. The mitochondrial permeability transition pore and its role in myocardial ischemia reperfusion injury[J].J Mol Cell Cardiol, 2015,78.-23-34.
  • 6Zhao ZQ, Corvera JS, Halkos ME, et al. Inhibition ofmyocardial injury by ischemic postconditioning during reperfusion: comparison with ischemic preconditioning[J]. Am J Physiol Heart Circ Physiol, 2003,285 (2) : H579-588.
  • 7Watanabe T, Niwa K, Niinuma H. Efficacy of postconditioning combined thrombus aspiration in patients with ST-segment elevation myocardial infarction[J]. JACC, 2012,59(13) : E471.
  • 8Burley DS, Baxter GF. Pharmacological targets revealed by myocardial postconditioning[J]. Curr Opin Pharmacol, 2009,9 (2) : 177-188.
  • 9Jain MV, Paezulla AM, Klonisch T, et al. Intereonnections between apoptotic, autophagic and necrotic pathways: implications for cancer therapy development[J]. J Cell Mol Med,2013,17(1) ,12-29.
  • 10王一茗,孙忠人.艾灸预处理对心肌缺血高脂血症大鼠心肌RyR2 mRNA的影响[J].中华中医药杂志,2011,26(5):1164-1167. 被引量:7

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