Skeletal muscle wasting in cachexia and sarcopenia: molecular pathophysiology and impact of exercise training.
Skeletal muscle wasting in cachexia and sarcopenia: molecular pathophysiology and impact of exercise training.
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DOI：
10.1007/s13539-010-0007-1
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发表时间：
2010-09
影响因子：
8.9
通讯作者：
Adams, Volker
中科院分区：
文献类型：
--
作者：
Lenk, Karsten;Schuler, Gerhard;Adams, Volker
骨骼肌是人体中最丰富的组织，维持其质量对于保证运动、力量和呼吸等基本功能至关重要。合成或分解骨骼肌蛋白的决定受信号通路网络的调节，该网络将外部刺激传递给调节基因转录的细胞内因子。肌肉蛋白分解和合成的严格调节平衡在几种不同的肌病中受到干扰，但也在两种病理中受到干扰：肌肉减少症和恶病质。近年来，我们发现在这两种肌肉萎缩疾病中，特定的调节分子（如泛素-蛋白酶体系统成员、肌肉生长抑制素、凋亡诱导因子）的表达增加，而其他因子（如胰岛素样生长因子1）的表达下调。到目前为止，还没有很多治疗方法可以对抗肌肉损失。最有希望的方法之一是运动训练，由于它的多因素影响，可以作用于几种信号通路。因此，这篇综述将集中在目前文献中讨论的两种肌肉萎缩疾病的骨骼肌中存在的特定改变。此外，我们将重点关注运动训练作为一种干预策略。
Skeletal muscle is the most abundant tissue in the human body, and the maintenance of its mass is essential to ensure basic function as locomotion, strength and respiration. The decision to synthesize or to break down skeletal muscle proteins is regulated by a network of signaling pathways that transmit external stimuli to intracellular factors regulating gene transcription. The tightly regulated balance of muscle protein breakdown and synthesis is disturbed in several distinct myopathies, but also in two pathologies: sarcopenia and cachexia. In recent years, it became evident that in these two muscle wasting disorders specific regulating molecules are increased in expression (e.g. members of the ubiquitin–proteasome system, myostatin, apoptosis inducing factors), whereas other factors (e.g. insulin-like growth factor 1) are down-regulated. So far, not many treatment options to fight the muscle loss are available. One of the most promising approaches is exercise training that, due to its multifactorial effects, can act on several signaling pathways. Therefore, this review will concentrate on specific alterations discussed in the current literature that are present in the skeletal muscle of both muscle wasting disorders. In addition, we will focus on exercise training as an intervention strategy.
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