Pestronk Alan, Keeling Richard, Choksi Rati
Department of Neurology, Washington University School of Medicine, 660 South Euclid Avenue, Box 8111, Saint Louis, Missouri, 63110, USA.
Department of Pathology and Immunology, Washington University School of Medicine, Saint Louis, Missouri, USA.
Muscle Nerve. 2017 Jul;56(1):122-128. doi: 10.1002/mus.25442. Epub 2017 Feb 8.
We studied mitochondrial impairment as a factor in the pathologic equivalent of sarcopenia, muscle fiber atrophy associated with increased age.
Mitochondrial oxidative enzyme activities and coenzyme Q10 levels were measured in frozen human proximal limb muscles with combined age and atrophy, age alone, atrophy alone, denervation, immune myopathies, and mitochondrial disorders with ophthalmoplegia.
Sarcopenia (age and atrophy) had reduced mean activities of mitochondrial Complexes I, II, and II+III, with severe reduction of Complex I activity in 54% of patients. Atrophy, and specific denervation atrophy, had similar patterns of changes. Age alone had moderately reduced Complex I activity. Mitochondrial myopathies had mildly lower Complex IV activity. Immune myopathies had unchanged enzyme activities.
Mitochondrial oxidative enzyme activities, especially Complex I, but also Complexes II and II+III, are reduced in muscles with the pathologic equivalent of sarcopenia. Individually, atrophy and age have different patterns of oxidative enzyme changes. Muscle Nerve 56: 122-128, 2017.
我们研究了线粒体损伤作为与肌肉减少症病理等效的一个因素，肌肉减少症是与年龄增长相关的肌纤维萎缩。
在患有年龄和萎缩合并症、单纯年龄增长、单纯萎缩、去神经支配、免疫性肌病以及伴有眼肌麻痹的线粒体疾病的人类近端肢体冷冻肌肉中，测量线粒体氧化酶活性和辅酶Q10水平。
肌肉减少症（年龄和萎缩）患者的线粒体复合物I、II以及II + III的平均活性降低，54%的患者复合物I活性严重降低。单纯萎缩以及特定的去神经支配性萎缩具有相似的变化模式。单纯年龄增长使复合物I活性中度降低。线粒体肌病患者的复合物IV活性轻度降低。免疫性肌病患者的酶活性未发生变化。
在与肌肉减少症病理等效的肌肉中，线粒体氧化酶活性降低，尤其是复合物I，还有复合物II和II + III。单独来看，萎缩和年龄增长具有不同的氧化酶变化模式。《肌肉与神经》56: 122 - 128, 2017年。
