Cardoso Susana, Correia Sónia, Carvalho Cristina, Candeias Emanuel, Plácido Ana I, Duarte Ana I, Seiça Raquel M, Moreira Paula I
CNC-Center for Neuroscience and Cell Biology, University of Coimbra, 3004-504, Coimbra, Portugal.
J Bioenerg Biomembr. 2015 Apr;47(1-2):119-31. doi: 10.1007/s10863-014-9580-x. Epub 2014 Sep 14.
The integrity of mitochondrial function is essential to cell life. It follows that disturbances of mitochondrial function will lead to disruption of cell function, expressed as disease or even death. Considering that neuronal uncoupling proteins (UCPs) decrease reactive oxygen species (ROS) production at the expense of energy production, it is important to understand the underlying mechanisms by which UCPs control the balance between the production of adenosine triphosphate (ATP) and ROS in the context of normal physiological activity and in pathological conditions. Here we review the current understanding of neuronal UCPs-mediated respiratory uncoupling process by performing a survey in their physiology and regulation. The latest findings regarding neuronal UCPs physiological roles and their involvement and interest as potential targets for therapeutic intervention in brain diseases will also be exploited.
线粒体功能的完整性对细胞生命至关重要。因此,线粒体功能紊乱将导致细胞功能破坏,表现为疾病甚至死亡。鉴于神经元解偶联蛋白(UCPs)以能量产生为代价减少活性氧(ROS)的产生,了解UCPs在正常生理活动和病理条件下控制三磷酸腺苷(ATP)和ROS产生之间平衡的潜在机制非常重要。在此,我们通过对神经元UCPs的生理学和调节进行综述,来阐述目前对其介导的呼吸解偶联过程的理解。还将探讨有关神经元UCPs生理作用的最新发现,以及它们作为脑部疾病治疗干预潜在靶点的相关性和研究价值。