Necroptosis in neurodegenerative diseases: a potential therapeutic target.
Necroptosis in neurodegenerative diseases: a potential therapeutic target.
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神经退行性疾病中的坏死性凋亡：潜在的治疗靶点
DOI：
10.1038/cddis.2017.286
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发表时间：
2017-06-29
影响因子：
9
通讯作者：
Xu YM
中科院分区：
文献类型：
--
作者：
Zhang S;Tang MB;Luo HY;Shi CH;Xu YM
神经退行性疾病是一组以神经元丢失为特征的慢性进行性疾病。坏死性凋亡是最近发现的一种程序性细胞死亡，是一种具有坏死样形态特征的细胞死亡机制。坏死性凋亡激活依赖于受体相互作用蛋白（RIP）同源相互作用基序（RHIM）。多种含RHIM的蛋白质将坏死凋亡信号从细胞触发物传递到细胞死亡介质RIP 3和混合谱系激酶结构域样蛋白（MLKL）。RIP 1在从细胞死亡激活到抑制的坏死性凋亡细胞死亡调节中起着特别重要和复杂的作用，并且这些功能通常是细胞类型和环境依赖性的。越来越多的证据表明，坏死性凋亡在神经退行性疾病的发病机制中起着重要作用。此外，小分子如坏死抑素-1被认为抑制坏死性凋亡信号通路。了解坏死性凋亡的确切机制及其与神经退行性疾病中其他细胞死亡途径的相互作用可以提供重要的治疗见解。本综述旨在总结坏死性凋亡的分子机制，并强调坏死性凋亡作为神经退行性疾病中神经元细胞死亡的主要驱动因素的新证据。
Neurodegenerative diseases are a group of chronic progressive disorders characterized by neuronal loss. Necroptosis, a recently discovered form of programmed cell death, is a cell death mechanism that has necrosis-like morphological characteristics. Necroptosis activation relies on the receptor-interacting protein (RIP) homology interaction motif (RHIM). A variety of RHIM-containing proteins transduce necroptotic signals from the cell trigger to the cell death mediators RIP3 and mixed lineage kinase domain-like protein (MLKL). RIP1 plays a particularly important and complex role in necroptotic cell death regulation ranging from cell death activation to inhibition, and these functions are often cell type and context dependent. Increasing evidence suggests that necroptosis plays an important role in the pathogenesis of neurodegenerative diseases. Moreover, small molecules such as necrostatin-1 are thought inhibit necroptotic signaling pathway. Understanding the precise mechanisms underlying necroptosis and its interactions with other cell death pathways in neurodegenerative diseases could provide significant therapeutic insights. The present review is aimed at summarizing the molecular mechanisms of necroptosis and highlighting the emerging evidence on necroptosis as a major driver of neuron cell death in neurodegenerative diseases.
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影响因子：
4.3
作者：
Farfel-Becker T;Vitner EB;Futerman AH
通讯作者：
Futerman AH
影响因子：
9
作者：
Cougnoux A;Cluzeau C;Mitra S;Li R;Williams I;Burkert K;Xu X;Wassif CA;Zheng W;Porter FD
通讯作者：
Porter FD
影响因子：
8
作者：
Challa, Sreerupa;Chan, Francis Ka-Ming
通讯作者：
Chan, Francis Ka-Ming
DOI：
10.1126/science.aaa3650
发表时间：
2015-03-27
期刊：
Science (New York, N.Y.)
影响因子：
--
作者：
Cirulli ET;Lasseigne BN;Petrovski S;Sapp PC;Dion PA;Leblond CS;Couthouis J;Lu YF;Wang Q;Krueger BJ;Ren Z;Keebler J;Han Y;Levy SE;Boone BE;Wimbish JR;Waite LL;Jones AL;Carulli JP;Day-Williams AG;Staropoli JF;Xin WW;Chesi A;Raphael AR;McKenna-Yasek D;Cady J;Vianney de Jong JM;Kenna KP;Smith BN;Topp S;Miller J;Gkazi A;FALS Sequencing Consortium;Al-Chalabi A;van den Berg LH;Veldink J;Silani V;Ticozzi N;Shaw CE;Baloh RH;Appel S;Simpson E;Lagier-Tourenne C;Pulst SM;Gibson S;Trojanowski JQ;Elman L;McCluskey L;Grossman M;Shneider NA;Chung WK;Ravits JM;Glass JD;Sims KB;Van Deerlin VM;Maniatis T;Hayes SD;Ordureau A;Swarup S;Landers J;Baas F;Allen AS;Bedlack RS;Harper JW;Gitler AD;Rouleau GA;Brown R;Harms MB;Cooper GM;Harris T;Myers RM;Goldstein DB
通讯作者：
Goldstein DB
影响因子：
8.8
作者：
Dondelinger, Yves;Declercq, Wim;Vandenabeele, Peter
通讯作者：
Vandenabeele, Peter