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The emerging role of Piezo1 channels in skeletal muscle physiology
Piezo1 channels are mechanically activated (MA) cation channels that are involved in sensing of various mechanical perturbations, such as membrane stretch and shear stress, and play a crucial role in cell mechanotransduction. In response to mechanical stimuli, these channels open up and allow cation...
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Published in: | Biophysical reviews 2023-10, Vol.15 (5), p.1171-1184 |
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Main Author: | |
Format: | Article |
Language: | English |
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Citations: | Items that this one cites Items that cite this one |
Online Access: | Get full text |
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Summary: | Piezo1 channels are mechanically activated (MA) cation channels that are involved in sensing of various mechanical perturbations, such as membrane stretch and shear stress, and play a crucial role in cell mechanotransduction. In response to mechanical stimuli, these channels open up and allow cations to travel into the cell and induce biochemical reactions that can change the cell’s metabolism and function. Skeletal muscle cells/fibers inherently depend upon mechanical cues in the form of fluid shear stress and contractions (physical exercise). For example, an exposure of skeletal muscles to chronic mechanical loading leads to increased anabolism and fiber hypertrophy, while prolonged mechanical unloading results in muscle atrophy. MA Piezo1 channels have recently emerged as key mechanosensors that are capable of linking mechanical signals and intramuscular signaling in skeletal muscle cells/fibers. This review will summarize the emerging role of Piezo1 channels in the development and regeneration of skeletal muscle tissue as well as in the regulation of skeletal muscle atrophy. In addition, an overview of potential Piezo1-related signaling pathways underlying anabolic and catabolic processes will be provided. A better understanding of Piezo1’s role in skeletal muscle mechanotransduction may represent an important basis for the development of therapeutic strategies for maintaining muscle functions under disuse conditions and in some disease states. |
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ISSN: | 1867-2450 1867-2469 |
DOI: | 10.1007/s12551-023-01154-6 |