Skeletal muscle mitochondrial depletion and dysfunction in chronic kidney disease.
Skeletal muscle mitochondrial depletion and dysfunction in chronic kidney disease.
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发表时间：
2013-08
影响因子：
0.1
通讯作者：
P. G. Yazdi;H. Moradi;Jia-Ying Yang;Ping H. Wang;N. Vaziri
中科院分区：
文献类型：
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作者：
P. G. Yazdi;H. Moradi;Jia-Ying Yang;Ping H. Wang;N. Vaziri
晚期慢性肾脏病（CKD）与运动能力受损、骨骼肌功能障碍和氧化应激有关。线粒体是能量产生和活性氧（ROS）产生的主要来源。在5/6肾切除术（CKD）或假手术（对照）后14周，测定雄性SD大鼠腓肠肌线粒体状态3呼吸、线粒体复合物I酶活性和组织孔蛋白/肌动蛋白比率。CKD组表现出氮质血症、高血压、状态3线粒体呼吸的显著降低（~ 39%）和线粒体复合物I酶活性的显著增加。后者是氧化磷酸化的第一步，这是一个与ROS产生有关的过程。这些异常与肌孔蛋白/β肌动蛋白比值显著降低相关，表明CKD动物骨骼肌中线粒体质量显著降低。CKD导致骨骼肌中线粒体呼吸受损、肌肉线粒体质量减少、能量产生降低和ROS产生增加。这些事件可以同时导致CKD患者运动能力和氧化应激的降低。
Advanced chronic kidney disease (CKD) is associated with impaired exercise capacity, skeletal muscle dysfunction, and oxidative stress. Mitochondria are the primary source for energy production and generation of reactive oxygen species (ROS). Mitochondrial state 3 respiration, mitochondrial complex I enzyme activity, and tissue porin/actin ratio were determined in the gastrocnemius muscle of male SD rats 14 weeks after 5/6 nephrectomy (CKD) or sham-operation (control). The CKD group exhibited azotemia, hypertension, significant reduction (-39%) of state 3 mitochondrial respiration, and a significant increase in the mitochondrial complex I enzyme activity. The latter is the first step in oxidative phosphorylation, a process linked to production of ROS. These abnormalities were associated with a significant reduction in muscle porin/β actin ratio denoting substantial reduction of mitochondrial mass in skeletal muscle of animals with CKD. CKD results in impaired mitochondrial respiration, reduced muscle mitochondrial mass, depressed energy production and increased ROS generation in the skeletal muscle. These events can simultaneously contribute to the reduction of exercise capacity and oxidative stress in CKD.