Magnetic stimulation supports muscle and nerve regeneration after trauma in mice

ABSTRACT Introduction: Magnetic stimulation (MS) has the ability to induce muscle twitch and has long been proposed as a therapeutic modality for skeletal muscle diseases. However, the molecular mechanisms underlying its means of action have not been defined. Methods: Muscle regeneration after traum...

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Published inMuscle & nerve Vol. 53; no. 4; pp. 598 - 607
Main Authors StÖlting, Meline N.L., Arnold, Anne Sophie, Haralampieva, Deana, Handschin, Christoph, Sulser, Tullio, Eberli, Daniel
Format Journal Article
LanguageEnglish
Published United States Blackwell Publishing Ltd 01.04.2016
Wiley Subscription Services, Inc
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Summary:ABSTRACT Introduction: Magnetic stimulation (MS) has the ability to induce muscle twitch and has long been proposed as a therapeutic modality for skeletal muscle diseases. However, the molecular mechanisms underlying its means of action have not been defined. Methods: Muscle regeneration after trauma was studied in a standard muscle injury mouse model. The influence of MS on the formation of motor units, posttrauma muscle/nerve regeneration, and vascularization was investigated. Results: We found that MS does not cause systemic or muscle damage but improves muscle regeneration by significantly minimizing the presence of inflammatory infiltrate and formation of scars after trauma. It avoids posttrauma muscle atrophy, induces muscle hypertrophy, and increases the metabolism and turnover of muscle. It triples the expression of muscle markers and significantly improves muscle functional recovery after trauma. Conclusions: Our results indicate that MS supports muscle and nerve regeneration by activating muscle–nerve cross‐talk and inducing the maturation of neuromuscular junctions. Muscle Nerve 53: 598–607, 2016
Bibliography:ark:/67375/WNG-LGVNV0F0-W
istex:BEF8B7E7C29924C7C596179D3B91D142BD5F061D
ArticleID:MUS24780
This study was supported by the Swiss National Foundation and the University of Zürich.
ObjectType-Article-1
SourceType-Scholarly Journals-1
ObjectType-Feature-2
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ISSN:0148-639X
1097-4598
DOI:10.1002/mus.24780