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Mitochondrial Nuclear Receptors and Transcription Factors: Who’s Minding the Cell?

机译:线粒体核受体和转录因子:谁介导细胞?

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摘要

Mitochondria are a power organelles generating biochemical energy, ATP, in the cell. Mitochondria play a variety of roles that include integrating extracellular signals and executing critical intracellular events, such as neuronal cell survival and death. Increasing evidence suggests that a cross-talk mechanism between mitochondria and the nucleus is closely related to neuronal function and activity. Nuclear receptors (estrogen receptors, thyroid (T3) hormone receptor, peroxisome proliferators-activated receptor gamma2) and transcription factors (cAMP response binding protein, p53) have been found to target mitochondria and exert pro-survival and pro-death pathways. In this context, the regulation of mitochondrial function via the translocation of nuclear receptors and transcription factors may underlie some of the mechanisms involved in neuronal survival and death. Understanding the function of nuclear receptors and transcription factors in the mitochondria may provide important pharmacological utility in the treatment of neurodegenerative conditions. Thus, the modulation of signaling pathways via mitochondria-targeting nuclear receptors and transcription factors is rapidly emerging as a novel therapeutic target.
机译:线粒体是在细胞中产生生化能ATP的动力细胞器。线粒体发挥多种作用,包括整合细胞外信号和执行关键的细胞内事件,例如神经元细胞的存活和死亡。越来越多的证据表明,线粒体与细胞核之间的串扰机制与神经元功能和活性密切相关。已发现核受体(雌激素受体,甲状腺(T3)激素受体,过氧化物酶体增殖物激活的受体γ2)和转录因子(cAMP反应结合蛋白,p53)靶向线粒体并发挥促生存和促死亡途径。在这种情况下,通过核受体和转录因子的易位来调节线粒体功能可能是神经元存活和死亡所涉及的一些机制的基础。了解线粒体中核受体和转录因子的功能可能在神经退行性疾病的治疗中提供重要的药理学用途。因此,经由靶向线粒体的核受体和转录因子的信号传导途径的调节作为新的治疗靶标迅速出现。

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