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Comparative Microarray Analysis Identifies Commonalities in Neuronal Injury: Evidence for Oxidative Stress, Dysfunction of Calcium Signalling, and Inhibition of Autophagy-Lysosomal Pathway

机译:比较微阵列分析确定神经元损伤的共性:氧化应激、钙信号传导功能障碍和自噬-溶酶体通路抑制的证据

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摘要

Mitochondrial dysfunction, ubiquitin-proteasomal system impairment and excitotoxicity occur during the injury and death of neurons in neurodegenerative conditions. The aim of this work was to elucidate the cellular mechanisms that are universally altered by these conditions. Through overlapping expression profiles of rotenone-, lactacystin- and N-methyl-d-aspartate-treated cortical neurons, we have identified three affected biological processes that are commonly affected; oxidative stress, dysfunction of calcium signalling and inhibition of the autophagic-lysosomal pathway. These data provides many opportunities for therapeutic intervention in neurodegenerative conditions, where mitochondrial dysfunction, proteasomal inhibition and excitotoxicity are evident.
机译:线粒体功能障碍、泛素-蛋白酶体系统损伤和兴奋性毒性发生在神经退行性疾病中神经元的损伤和死亡期间。这项工作的目的是阐明这些条件普遍改变的细胞机制。通过鱼藤酮、乳囊蛋白和 N-甲基-d-天冬氨酸处理的皮质神经元的重叠表达谱,我们确定了三种通常受影响的生物过程;氧化应激、钙信号传导功能障碍和自噬溶酶体途径抑制。这些数据为神经退行性疾病的治疗干预提供了许多机会,其中线粒体功能障碍、蛋白酶体抑制和兴奋性毒性很明显。

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