中国科技核心期刊
CN:31-1600/Q
ISSN:1004-0374
“健康与疾病的免疫”国际学术研讨会通知      关于有网站冒充本刊网站的声明
《生命科学》 2015, 27(7): 922-927
解偶联蛋白与阿尔茨海默病
张 军1,于 霄1,郭 羽1,吴 琼2,邹 原2*
(1 大连医科大学病理学教研室,大连 116044;2 大连医科大学生理学教研室,大连 116044)
摘 要:解偶联蛋白(uncoupling protein, UCP) 是线粒体内膜上的质子转运蛋白,被激活时能引发质子漏,质子经UCP 渗漏回基质,使氧化磷酸化部分解耦联,降低线粒体膜电位,减少过量活性氧的产生。另外,UCP 对ATP 合成、钙离子稳态、能量代谢等也有调节作用。阿尔茨海默病是一种中枢神经系统退行性疾病,由多种因素共同作用引起,其中活性氧的作用越来越引起重视。UCP,特别是UCP2 在中枢神经系统疾病方面的保护作用日益引起关注,有望成为阿尔茨海默病治疗的靶向目标。
 
Uncoupling protein and Alzheimer’s disease
ZHANG Jun1, YU Xiao1, GUO Yu1, WU Qiong2, ZOU Yuan2*
(1 Department of Pathology, Dalian Medical University, Dalian 116044, China; 2 Department of Physiology, Dalian Medical University, Dalian 116044, China)
Abstract: Uncoupling protein (UCP) is the mitochondrial inner membrane carrier protein. When the concept of mild uncoupling has been introduced, UCP predicts the existence of a protein-regulated proton leak with the main purpose of controlling mitochondrial oxidative stress, and reducing the generation of superoxide anion. In addition, UCP interferes with ATP synthesis, as a potential modulator of mitochondrial Ca2+ uptake and energy metabolism. Alzheimer’s disease (AD) is progressively neurodegenerative disorder. A large number of studies have shown that reactive oxygen species (ROS) plays a significant role in AD pathogenesis. UCP has an important impact on mitochondrial ROS production, ATP generation and calcium regulation, suggesting that UCP, especially UCP2, may be a potential target for AD treatment.
 
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