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Front Physiol. 2020 Oct 22;11:595800. doi: 10.3389/fphys.2020.595800. eCollection 2020.
2
Active acetylcholine receptors prevent the atrophy of skeletal muscles and favor reinnervation.乙酰胆碱受体的激活可防止骨骼肌萎缩,并有利于神经再支配。
Nat Commun. 2020 Feb 26;11(1):1073. doi: 10.1038/s41467-019-14063-8.
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P2X7 activation enhances skeletal muscle metabolism and regeneration in SOD1G93A mouse model of amyotrophic lateral sclerosis.P2X7 受体的激活可增强 SOD1G93A 肌萎缩侧索硬化症小鼠模型的骨骼肌代谢和再生。
Brain Pathol. 2020 Mar;30(2):272-282. doi: 10.1111/bpa.12774. Epub 2019 Aug 18.
4
Dysregulated mitochondrial Ca and ROS signaling in skeletal muscle of ALS mouse model.肌萎缩侧索硬化症小鼠模型中线粒体钙和 ROS 信号的失调。
Arch Biochem Biophys. 2019 Mar 15;663:249-258. doi: 10.1016/j.abb.2019.01.024. Epub 2019 Jan 22.
5
ROS-related mitochondrial dysfunction in skeletal muscle of an ALS mouse model during the disease progression.肌萎缩侧索硬化症模型小鼠疾病进展过程中与 ROS 相关的骨骼肌线粒体功能障碍。
Pharmacol Res. 2018 Dec;138:25-36. doi: 10.1016/j.phrs.2018.09.008. Epub 2018 Sep 18.
6
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7
The excitation-contraction coupling mechanism in skeletal muscle.骨骼肌中的兴奋-收缩偶联机制。
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Absence of physiological Ca transients is an initial trigger for mitochondrial dysfunction in skeletal muscle following denervation.生理性钙瞬变的缺失是去神经支配后骨骼肌线粒体功能障碍的初始触发因素。
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钙介导的骨骼肌神经肌肉接头和线粒体之间的偶联。

Ca-mediated coupling between neuromuscular junction and mitochondria in skeletal muscle.

机构信息

Department of Kinesiology, College of Nursing and Health Innovation, University of Texas at Arlington, Arlington, TX 76010, USA.

出版信息

Neurosci Lett. 2021 May 29;754:135899. doi: 10.1016/j.neulet.2021.135899. Epub 2021 Apr 15.

DOI:10.1016/j.neulet.2021.135899
PMID:33865940
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8089061/
Abstract

The volitional movement of skeletal is controlled by the motor neuron at the site of neuromuscular junction (NMJ) where the retrograde signals are also passed back from muscle to the motor neuron. As the normal function of muscle largely depends on mitochondria that determine the fate of a skeletal muscle myofiber, there must exist a fine-controlled functional coupling between NMJ and mitochondria in myofibers. This mini-review discusses recent publications that reveal how spatiotemporal profiles of intracellular free Ca could couple mitochondrial function with the activity of NMJ in skeletal muscle myofibers.

摘要

骨骼的随意运动受运动神经元控制,运动神经元位于神经肌肉接头(NMJ)处,逆行信号也从肌肉传递回运动神经元。由于肌肉的正常功能在很大程度上取决于决定骨骼肌肌纤维命运的线粒体,因此 NMJ 和肌纤维中线粒体之间必须存在精细控制的功能偶联。这篇小综述讨论了最近的出版物,揭示了细胞内游离 Ca 的时空分布如何将线粒体功能与骨骼肌肌纤维中 NMJ 的活性偶联起来。