Yap Yann Wan, Llanos Roxana M, La Fontaine Sharon, Cater Michael A, Beart Philip M, Cheung Nam Sang
Centre for Cellular and Molecular Biology, School of Life and Environmental Sciences, Deakin University, Burwood, VIC, 3125, Australia.
Florey Institute of Neuroscience and Mental Health, University of Melbourne, Parkville, VIC, 3052, Australia.
Neurochem Res. 2016 Mar;41(3):554-67. doi: 10.1007/s11064-015-1666-2. Epub 2015 Aug 29.
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.
在神经退行性疾病中，神经元损伤和死亡过程中会出现线粒体功能障碍、泛素-蛋白酶体系统损伤和兴奋性毒性。这项工作的目的是阐明受这些情况普遍影响的细胞机制。通过鱼藤酮、乳胞素和N-甲基-D-天冬氨酸处理的皮质神经元的重叠表达谱，我们确定了三个共同受到影响的生物学过程；氧化应激、钙信号功能障碍和自噬-溶酶体途径的抑制。这些数据为神经退行性疾病的治疗干预提供了许多机会，在这些疾病中，线粒体功能障碍、蛋白酶体抑制和兴奋性毒性很明显。
