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通过机械激活离子通道进行肌肉蛋白质合成的机械转导

Mechanotransduction for Muscle Protein Synthesis via Mechanically Activated Ion Channels.

作者信息

Mirzoev Timur M

机构信息

Myology Laboratory, Institute of Biomedical Problems RAS, 123007 Moscow, Russia.

出版信息

Life (Basel). 2023 Jan 27;13(2):341. doi: 10.3390/life13020341.


DOI:10.3390/life13020341
PMID:36836698
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9962945/
Abstract

Cell mechanotransduction, the ability to detect physical forces and convert them into a series of biochemical events, is important for a wide range of physiological processes. Cells express an array of mechanosensors transducing physical forces into intracellular signaling cascades, including ion channels. Ion channels that can be directly activated by mechanical cues are known as mechanically activated (MA), or stretch-activated (SA), channels. In response to repeated exposures to mechanical stimulation in the form of resistance training, enhanced protein synthesis and fiber hypertrophy are elicited in skeletal muscle, whereas a lack of mechanical stimuli due to inactivity/mechanical unloading leads to reduced muscle protein synthesis and fiber atrophy. To date, the role of MA channels in the transduction of mechanical load to intracellular signaling pathways regulating muscle protein synthesis is poorly described. This review article will discuss MA channels in striated muscle, their regulation, and putative roles in the anabolic processes in muscle cells/fibers in response to mechanical stimuli.

摘要

细胞机械转导,即检测物理力并将其转化为一系列生化事件的能力,对广泛的生理过程至关重要。细胞表达一系列机械传感器,将物理力转化为细胞内信号级联反应,其中包括离子通道。可被机械信号直接激活的离子通道被称为机械激活(MA)通道或牵张激活(SA)通道。骨骼肌在反复接受以阻力训练形式出现的机械刺激后,会引发蛋白质合成增强和纤维肥大,而因不活动/机械卸载导致缺乏机械刺激则会导致肌肉蛋白质合成减少和纤维萎缩。迄今为止,MA通道在将机械负荷转导至调节肌肉蛋白质合成的细胞内信号通路中的作用鲜有描述。这篇综述文章将讨论横纹肌中的MA通道、它们的调节以及在肌肉细胞/纤维响应机械刺激的合成代谢过程中的假定作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0731/9962945/9c31f2ddc36b/life-13-00341-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0731/9962945/318403f69ac6/life-13-00341-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0731/9962945/9c31f2ddc36b/life-13-00341-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0731/9962945/318403f69ac6/life-13-00341-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0731/9962945/9c31f2ddc36b/life-13-00341-g002.jpg

相似文献

[1]
Mechanotransduction for Muscle Protein Synthesis via Mechanically Activated Ion Channels.

Life (Basel). 2023-1-27

[2]
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[3]
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[4]
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[9]
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[10]
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[3]
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[4]
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[5]
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本文引用的文献

[1]
A preliminary study on the role of Piezo1 channels in myokine release from cultured mouse myotubes.

Biochem Biophys Res Commun. 2022-10-1

[2]
A Piezo1/KLF15/IL-6 axis mediates immobilization-induced muscle atrophy.

J Clin Invest. 2022-5-16

[3]
Tethering Piezo channels to the actin cytoskeleton for mechanogating via the cadherin-β-catenin mechanotransduction complex.

Cell Rep. 2022-2-8

[4]
Why exercise builds muscles: titin mechanosensing controls skeletal muscle growth under load.

Biophys J. 2021-9-7

[5]
"Time window" effect of Yoda1-evoked Piezo1 channel activity during mouse skeletal muscle differentiation.

Acta Physiol (Oxf). 2021-12

[6]
The Role of GSK-3β in the Regulation of Protein Turnover, Myosin Phenotype, and Oxidative Capacity in Skeletal Muscle under Disuse Conditions.

Int J Mol Sci. 2021-5-11

[7]
How Postural Muscle Senses Disuse? Early Signs and Signals.

Int J Mol Sci. 2020-7-16

[8]
TRPCs: Influential Mediators in Skeletal Muscle.

Cells. 2020-4-1

[9]
An Anabolic Signaling Response of Rat Soleus Muscle to Eccentric Contractions Following Hindlimb Unloading: A Potential Role of Stretch-Activated Ion Channels.

Int J Mol Sci. 2019-3-7

[10]
The skeletal muscle fiber: a mechanically sensitive cell.

Eur J Appl Physiol. 2019-1-5

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