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ER stress in skeletal muscle remodeling and myopathies

机译：ER骨骼肌重塑和肌病的反应

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摘要

Skeletal muscle is a highly plastic tissue in the human body that undergoes extensive adaptation in response to environmental cues, such as physical activity, metabolic perturbation, and disease conditions. The endoplasmic reticulum (ER) plays a pivotal role in protein folding and calcium homeostasis in many mammalian cell types, including skeletal muscle. However, overload of misfolded or unfolded proteins in the ER lumen cause stress, which results in the activation of a signaling network called the unfolded protein response (UPR). The UPR is initiated by three ER transmembrane sensors: protein kinase R-like endoplasmic reticulum kinase, inositol-requiring protein 1 alpha, and activating transcription factor 6. The UPR restores ER homeostasis through modulating the rate of protein synthesis and augmenting the gene expression of many ER chaperones and regulatory proteins. However, chronic heightened ER stress can also lead to many pathological consequences including cell death. Accumulating evidence suggests that ER stress-induced UPR pathways play pivotal roles in the regulation of skeletal muscle mass and metabolic function in multiple conditions. They have also been found to be activated in skeletal muscle under catabolic states, degenerative muscle disorders, and various types of myopathies. In this article, we have discussed the recent advancements toward understanding the role and mechanisms through which ER stress and individual arms of the UPR regulate skeletal muscle physiology and pathology.
机译：骨骼肌是人体中高度塑料的组织，以响应环境提示，例如身体活动，代谢扰动和疾病条件，经历广泛的适应性。内质网（ER）在许多哺乳动物细胞类型中在蛋白质折叠和钙稳态中起着枢轴作用，包括骨骼肌。然而，ER管腔中错误折叠或展开蛋白质的过载导致应力，这导致激活称为展开蛋白质反应的信号网络（UPR）。 UPR由三种ER跨膜传感器引发：蛋白激酶R样内质网激酶，需要蛋白质1α和激活转录因子6. UPR通过调节蛋白质合成速率并增强基因表达来恢复ER稳态许多伴侣和调节蛋白。然而，慢性加强的ER压力也可能导致许多病理后果，包括细胞死亡。累积证据表明，ER应激诱导的UPR途径在多种条件下调节骨骼肌质量和代谢功能的调节中的枢转作用。他们也被发现在分解代谢态，退化肌病和各种肌病下在骨骼肌中被激活。在本文中，我们讨论了解uPR调节骨骼肌生理学和病理学的厄尔应激和单个武器的作用和机制的最新进步。

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