Type 2 Transglutaminase, mitochondria and Huntington's disease: Menage a trois
Type 2 Transglutaminase, mitochondria and Huntington's disease: Menage a trois
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DOI：
10.1016/j.mito.2014.09.008
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发表时间：
2014-11-01
期刊：
影响因子：
4.4
通讯作者：
Campanella, Michelangelo
中科院分区：
文献类型：
--
作者：
Altuntas, Sara;D'Eletto, Manuela;Campanella, Michelangelo
线粒体产生大量的细胞能量，并通过整合不同的输入信号作为细胞反应的决定性“枢纽”。作为哺乳动物生理病理学的决定因素，它们因其对脑退化的贡献而引起人们的关注。它们如何能够承受或屈服于导致神经元死亡的侮辱是一个非常关注的对象，增加了更好地了解胞质溶胶中的内部和外部线粒体通路之间的相互作用的需要。在后者中，那些决定蛋白质代谢并因此影响细胞器的质量功能和控制的蛋白质代谢是我们最直接的兴趣，在这里我们描述了2型转谷氨酰胺酶（TG 2）对线粒体功能、功能障碍和神经退行性变的贡献。除了回顾最新的证据，我们还分享了IF1途径的新证据，描绘了一个管理线粒体周转和稳态的分子管道，与设想预防和治疗策略相关，分别预测和抵消与神经病理学中线粒体功能失调相关的缺陷。(C)2014 Elsevier B.V.和线粒体研究学会。All rights reserved.
Mitochondria produce the bulk of cellular energy and work as decisional "hubs" for cellular responses by integrating different input signals. The determinant in the physiopathology of mammals, they attract major attention, nowadays, for their contribution to brain degeneration. How they can withstand or succumb to insults leading to neuronal death is an object of great attention increasing the need for a better understanding of the interplay between inner and outer mitochondrial pathways residing in the cytosol. Of the latter, those dictating protein metabolism and therefore influencing the quality function and control of the organelle are of our most immediate interest and here we describe the Transglutaminase type 2 (TG2) contribution to mitochondrial function, dysfunction and neurodegeneration. Besides reviewing the latest evidences we share also the novel ones on the IF1 pathway depicting a molecular conduit governing mitochondrial turnover and homeostasis relevant to envisaging preventive and therapeutic strategies to respectively predict and counteract deficiencies associated with deregulated mitochondrial function in neuropathology. (C) 2014 Elsevier B.V. and Mitochondria Research Society. All rights reserved.