期刊文献+

Necroptosis的调控机制及其在组织及细胞缺血损伤中的作用和意义

Regulatory Mechanism and Important Role of Necroptosis in Tissue and Cell Ischemic Injury
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摘要 Necroptosis不同于坏死和凋亡,具有坏死的细胞形态特点和自噬的活化,并且是主动耗能的,是被一系列信号传导通路所调控的细胞死亡机制。Necroptosis的发现和确认为细胞死亡的逆转和治疗开创了一个新的研究和应用途经。RIPl激酶是调控Necroptosis形成的关键酶,Necrostatins则是一类小分子化合物,它通过特异性地抑制细胞RIPl激酶而抑制Necroptosis的形成。 Necroptosis is different from necrosis and apoptosis and characterized by necrotic cell death morphology and activation of autophagy. Necroptosis is an active and energy consuming cell death mechanism, which is regulated by a set of signal-transduction pathways. The discovery and i- dentification of necroptosis has initiated a new approach of research and application for cell death re- version and treatment. RIP1 kinase has been identified as a key enzyme to regulate necropto- sis. Necrostatins are one kind of small molecule compounds that specifically block the execution of necroptosis by inhibiting RIP1 kinase activity. In this review, we elucidate the execution and regula- tion of tissue and cell necroptosis from gene level, cellular level to animal models, to provide com- prehensive information and understanding of necroptosis.
出处 《医学分子生物学杂志》 CAS CSCD 2009年第6期547-549,共3页 Journal of Medical Molecular Biology
基金 资助项目:河南省杰出人才创新基金(No.074200510014)
关键词 坏死状凋亡 RIPI Necrostatins 组织缺血损伤 Necroptosis RIP1 Necrostatins tissue ischemic injury
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  • 1VANDENABEELE P, DECLERCQ W, BERGHE T V. Necrotic cell death and ' necrostatins' : now we can control cellular explosion [ J ]. Trends Biochem Sci,2008,33 ( 8 ) : 352-355.
  • 2DEGTEREV A, HUANG Z, BOYCE M, et al. Chemical inhibitor of nonapoptotic cell death with therapeutic potential for ischemic brain injury[ J]. Nat Chem Biol,2005,1 (2) :112-119.
  • 3KROEMER G, GALLUZZI L, VANDENABEELE P, et al. Classification of cell death: recommendations of the Nomenclature Committee on Cell death 2009 [ J ]. Celt Death Differ, 2009,16 ( 1 ) : 3-11.
  • 4DEGTEREV A, HITOMI J, GERMSCHEID M, et al. Identification of RIPI kinase as a specific cellular target of necrostatins[ J]. Nat Chem Biol,2008,4 ( 5 ) : 313-321.
  • 5GOLSTEIN P, KROEMER G. Cell death by necrosis:towards a molecular definition[ J]. Trends Bioehem Sci ,2007,32( 1 ) :37-43.
  • 6LIM S Y, DAVIDSON S M, MOCANU M M, el al. The cardioprotective effect of necrustat in requires the cyclophilin-O component of the mitochondrial permeability transition pore [ J ]. Cardiovasc Drugs Ther, 2007,21 ( 6 ) :467-469.
  • 7CAUWELS A,JANSSEN B, WAEYTENS A,et al. Caspase inhibition causes hyperacute tumor necrosis factor-induced shock via oxidative stress and phosphlipase A2 [ J ]. Nat Immunol,2003,4 (4) : 387-393.
  • 8BAO L, LI Y, DENG S X, et al. Sitosterol-containing lipoproteins trigger free sterol-induced caspase-independent death in ACAT- competent macrophages [ J ]. J Biol Chem, 2006,281 ( 44 ) : 33635- 33649.
  • 9GOZUACIK D,KIMCHI A. Autophagy as celt death and tumor suppressor mechanism [ J ]. Oncogene ,2004,23 ( 16 ) : 2891-2906.
  • 10XU X, CHUA C C , KONG J, et al. Necrostatin-1 protects against glutamate-induced glutathione depletion and caspase-independent cell death in HT-22 cells[ J ]. J Neurochem, 2007,103 ( 5 ) : 2004- 2014.

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