Catabolism of aging: is it an inflammatory process?
Catabolism of aging: is it an inflammatory process?
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DOI：
10.1097/01.mco.0000068965.34812.62
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发表时间：
2003-05-01
影响因子：
3.1
通讯作者：
Roubenoff, R
中科院分区：
文献类型：
--
作者：
Roubenoff, R
综述目的肌肉减少症领域的研究正在迅速发展，该过程现在被认为是老年人虚弱和发病的重要原因。这篇评论集中在该领域的最新发展，特别是关于分解代谢刺激的作用，在引起sarcopenias.Recent发现现在有一个令人印象深刻的机构的文献牵连增加白细胞介素-6水平在成功老龄化的成年人。新的数据表明，高水平的白细胞介素-6携带不良预后，虽然目前还不清楚，如果细胞因子主要有一个因果或反调节功能。白细胞介素-6和其他细胞因子可以通过直接分解代谢作用，或通过引起饮食能量摄入减少（衰老的厌食症），或通过诱导胰岛素抵抗或降低生长激素-胰岛素样生长因子-I浓度来发挥作用。此外，细胞凋亡现在已经与肌肉减少症，这表明，即使在没有明显的炎症性疾病的情况下，炎症信号也可能引发老年人肌肉细胞的损失。概要衰老导致许多存在于年轻成年期的肌肉合成代谢信号的损失。最近的研究表明，随着年龄的增长，分解代谢信号也会增加。
Purpose of review Research in the field of sarcopenia is evolving rapidly, and the process is now recognized as an important cause of frailty and morbidity in the elderly. This review focuses on recent developments in the field, especially regarding the role of catabolic stimuli in causing sarcopenia.Recent findings There is now an impressive body of literature implicating increased interleukin-6 levels in successfully aging adults. New data indicate that high interleukin-6 levels carry a poor prognosis, although it is not clear if the cytokine has primarily a causal or counter-regulatory function. Interleukin-6 and other cytokines could function through direct catabolic effects, or by causing reduced dietary energy intake (the anorexia of aging), or by inducing insulin resistance or lowering growth hormone-insulin-like growth factor-I concentrations. Furthermore, apoptosis has now been linked to sarcopenia, suggesting that an inflammatory signal could trigger loss of muscle cells in the elderly even in the absence of overt inflammatory disease.Summary Aging causes loss of many of the anabolic signals to muscle that are present in young adulthood. Recent research suggests that there is also an increase in catabolic signals with age.