Cross talk between SOD1 and the mitochondrial UPR in cancer and neurodegeneration
Cross talk between SOD1 and the mitochondrial UPR in cancer and neurodegeneration
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DOI：
10.1016/j.mcn.2019.04.003
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发表时间：
2019-07-01
影响因子：
3.5
通讯作者：
Germain, Doris
中科院分区：
文献类型：
--
作者：
Gomez, Maria;Germain, Doris
线粒体未折叠蛋白反应（UPRmt）正在迅速获得关注。虽然UPRmt的CHOP（ATF 4/5）轴是第一个被描述的，但随后报道了其他轴。在C.线虫已经被广泛研究。然而，UPRmt在已知涉及线粒体重编程或功能障碍的疾病（如癌症和神经变性）的小鼠模型中的验证才刚刚开始出现。这篇综述总结了最近的研究结果，并强调了超氧化物歧化酶SOD 1在线粒体和细胞核之间的通信在这些设置中的主要作用。虽然SOD 1主要是在家族性肌萎缩侧索硬化症（fALS）的背景下进行研究，但最近的研究表明，SOD 1可能是UPRmt的潜在重要介质，并集中强调SOD 1作为癌症治疗靶点的日益重要的作用。
The mitochondrial unfolded protein response (UPRmt) is rapidly gaining attention. While the CHOP (ATF4/5) axis of the UPRmt was the first to be described, other axes have subsequently been reported. Validation of this complex pathway in C. elegans has been extensively studied. However, validation of the UPRmt in mouse models of disease known to implicate mitochondrial reprogramming or dysfunction, such as cancer and neurodegeneration, respectively, is only beginning to emerge. This review summarizes recent findings and highlights the major role of the superoxide dismutase SOD1 in the communication between the mitochondria and the nucleus in these settings. While SOD1 has mostly been studied in the context of familial amyotrophic lateral sclerosis (fALS), recent studies suggest that SOD1 may be a potentially important mediator of the UPRmt and converge to emphasize an increasingly vital role of SOD1 as a therapeutic target in cancer.