Objective to observe the role of mitochondria dysfunction in neuron apoptosis during ischemia-reperfusion injury.
目的观察线粒体功能失调在缺血再灌后神经元凋亡中的作用。
One of the signs of ageing is weakening of skeletal muscles and increasing dysfunction of their mitochondria.
年老迹象之一是，骨骼肌的衰减及其线粒体的功能不良。
The dysfunction of mitochondria involves in the pathogenesis of shock and MODS.
线粒体功能紊乱参与了休克和多器官功能不全的发生。
Impairment of neuronal mitochondria following hypoxia of brain not only result in nerve cell's energy-deprivation and dysfunction, mitochondria also play key roles in apoptosis of neurons.
脑缺氧后神经元线粒体损伤不单使细胞发生能量缺失和功能丧失，还可以介导凋亡调节信号，是缺氧损伤后神经元凋亡的一个中心环节。
Dysfunction in mitochondria already is associated with a number of other neurological conditions, including Parkinson's disease, Alzheimer's disease, schizophrenia and bipolar disorder.
早有已有研究证明线粒体功能障碍与多种很多其他神经系统疾病，包括帕金森病、阿尔茨海默病、精神分裂症及双相情感障碍有关。
Dysfunction in mitochondria already is associated with a number of other neurological conditions, including Parkinson's disease, Alzheimer's disease, schizophrenia and bipolar disorder.
早有已有研究证明线粒体功能障碍与多种很多其他神经系统疾病，包括帕金森病、阿尔茨海默病、精神分裂症及双相情感障碍有关。
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