线粒体功能障碍在帕金森病中的研究进展

线粒体是细胞内广泛存在的膜性结构,参与诸多细胞活动,如产生能量、调节钙离子稳态、调控细胞程序性死亡等。神经元轴突和树突中存在着活跃的线粒体移动以促进细胞代谢及机体的正常功能。线粒体在维持神经元活力方面起着重要的作用,功能障碍的线粒体可以引起神经元功能障碍及细胞死亡。研究表明,线粒体功能障碍与帕金森病(PD)的病因和发病机制有关,无论线粒体功能障碍在PD中是原发事件还是继发事件,都能够为阻止PD的病理改变提供新的治疗靶点。

Mitochondrial Dysfunction and Parkinson Disease

Mitochondria are kinds of intracellular membrane-enclosed organelles,involved in a number of crucial cellular activities, such as the generation of energy as adenosine triphosphate, the regulation of calcium homeostasis, and programmed cell death. In neurons, mitochondria are actively transported throughout axons and dendrites to facilitate cellular metabolism and normal functions. Mitochondria are important for neuronal viability, and dysfunctional mitochondria can lead to neuron dysfunction and cell death. Defects in mitochon- drial function have long been suggested to be associated with the etiology and pathogenesis of Parkinson disease（PD）. No matter being a primary or subsequent event,mitochondrial dysfunction is a potential thera- peutic target to halt the pathological progression of PD.