Apoptosis in skeletal muscle with aging
Apoptosis in skeletal muscle with aging
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DOI：
10.1152/ajpregu.00458.2001
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发表时间：
2002-02-01
影响因子：
2.8
通讯作者：
Leeuwenburgh, C
中科院分区：
文献类型：
--
作者：
Dirks, A;Leeuwenburgh, C
肌肉减少症的部分原因可能是细胞凋亡导致的总纤维数量的损失。我们研究了6岁和24岁雄性Fisher 344大鼠腓肠肌线粒体介导途径中导致细胞凋亡的年龄相关改变。老龄大鼠腓肠肌细胞凋亡（单核小体和寡核小体分裂）比成年大鼠增加50%。此外，细胞质细胞色素c与caspase-3活性之间存在显著相关性，尽管细胞色素c和caspase-3活性均未随着年龄的增长而显著增加。此外，仅在老年大鼠中，caspase-3活性与单核小体和寡核小体断裂之间存在显著相关性。线粒体Bcl-2和Bax不随年龄变化。体外实验表明，骨骼肌中caspase级联的激活可能受到procaspase-9激活的限制。这是第一个探讨细胞凋亡在肌肉减少症中的作用的研究，并表明细胞凋亡的微妙变化参与其中。
Sarcopenia may be partly due to a loss in total fiber number by apoptosis. We have investigated age-related alterations in the mitochondria-mediated pathway leading to apoptosis in the gastrocnemius muscle from 6-mo-old and 24-mo-old male Fisher 344 rats. Apoptosis (mono- and oligonucleosome fragmentation) in the gastrocnemius muscle was increased by 50% in the old rats compared with the adult animals. Furthermore, there was a significant correlation between cytosolic cytochrome c and caspase-3 activity, although neither cytochrome c nor caspase-3 activity increased significantly with age. Furthermore, there was a significant correlation between caspase-3 activity and mono- and oligonucleosome fragmentation in the old rats only. Mitochondrial Bcl-2 and Bax were not altered with age. In vitro experiments demonstrated that activation of the caspase cascade in skeletal muscle might be limited by procaspase-9 activation. This is the first study to explore the role of apoptosis in sarcopenia and suggests that subtle changes in apoptosis are involved.