Emerging roles of ER stress and unfolded protein response pathways in skeletal muscle health and disease.
Emerging roles of ER stress and unfolded protein response pathways in skeletal muscle health and disease.
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DOI：
10.1002/jcp.25852
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发表时间：
2018-01
影响因子：
5.6
通讯作者：
Kumar A
中科院分区：
文献类型：
--
作者：
Bohnert KR;McMillan JD;Kumar A
骨骼肌是人体中最丰富的组织，可以根据身体活动、新陈代谢、生长因素和疾病状况来调整其质量。骨骼肌含有广泛的内质网（ER）网络，称为肌浆网，它在蛋白质平衡和钙稳态的调节中起重要作用。在许多细胞类型中，破坏内质网功能的环境和遗传因素会导致内质网管内错误折叠和未折叠蛋白质的积累，最终导致内质网应激。为了减轻压力和恢复体内平衡，内质网激活了一个称为未折叠蛋白反应（UPR）的信号网络。普遍定期审议有三个分支，分别调控多种内质网伴侣蛋白和调节蛋白的合成和表达。然而，个体UPR通路在骨骼肌中的作用才刚刚开始被研究。最近的研究表明，UPR通路在肌肉干细胞稳态、成肌分化和受伤骨骼肌再生中起着关键作用。此外，骨骼肌中的内质网应激和UPR标记在多种情况下被激活，如运动、去神经支配、饥饿、高脂肪饮食、癌症恶病质和衰老。越来越多的证据也表明内质网应激可能在炎症性肌病和遗传性肌肉疾病的发病机制中起重要作用。这篇综述文章的目的是讨论内质网应激和UPR的各个臂在各种生理和病理生理条件下调节骨骼肌形成、可塑性和功能的作用和潜在机制。
Skeletal muscle is the most abundant tissue in the human body and can adapt its mass as a consequence of physical activity, metabolism, growth factors, and disease conditions. Skeletal muscle contains an extensive network of endoplasmic reticulum (ER), called sarcoplasmic reticulum, which plays an important role in the regulation of proteostasis and calcium homeostasis. In many cell types, environmental and genetic factors that disrupt ER function cause an accumulation of misfolded and unfolded proteins in the ER lumen that ultimately leads to ER stress. To alleviate the stress and restore homeostasis, the ER activates a signaling network called the unfolded protein response (UPR). The UPR has three arms, which regulate protein synthesis and expression of many ER chaperone and regulatory proteins. However, the role of individual UPR pathways in skeletal muscle has just begun to be investigated. Recent studies suggest that UPR pathways play pivotal roles in muscle stem cell homeostasis, myogenic differentiation, and regeneration of injured skeletal muscle. Moreover, markers of ER stress and the UPR are activated in skeletal muscle in diverse conditions such as exercise, denervation, starvation, high fat diet, cancer cachexia, and aging. Accumulating evidence also suggests that ER stress may have important roles in the pathogenesis of inflammatory myopathies and genetic muscle disorders. The purpose of this review article is to discuss the role and potential mechanisms by which ER stress and the individual arms of the UPR regulate skeletal muscle formation, plasticity, and function in various physiological and pathophysiological conditions.
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