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Updated: Feb 11, 2026

Immunolabelling Myofiber Degeneration in Muscle Biopsies
Published on: December 5, 2019
Neuroimmune interactions in fascia and myofiber regeneration: a narrative review
Robbert N van Amstel1, Ivo J Lutke Schipholt2, Guido Weide1
1Laboratory for Myology, Department of Human Movement Sciences, Faculty of Behavioural and Movement Sciences, Vrije Universiteit Amsterdam, Amsterdam Movement Sciences, the Netherlands; Department of Human Movement Sciences, Faculty of Behavioural and Movement Sciences, Neuromechanics, Vrije Universiteit Amsterdam, Amsterdam Movement Sciences, the Netherlands.
Abstract:
When not treated adequately, neuromusculoskeletal, tendinous, and joint tissue injuries may become chronic, leading to impaired tissue function due to fibrosis, extracellular matrix densification, and fatty connective tissue accumulation, ultimately resulting in reduced joint and muscle mobility. Timely treatment involving the mobilization of fascia and targeted muscle exercise has been shown to enhance and promote tissue regeneration. Key phases in tissue regeneration after injury include the activation of the innate immune system, followed by its resolution. Although several treatment modalities are effective in restoring tissue function, their success rate and time to recovery may still need optimization. Over recent decades, increasing attention has been given to the role of fascia in neuromuscular tissue function, adaptation, and regeneration. However, the complex interactions between fasciae, myofibers, and the immune system remain insufficiently understood, particularly regarding the mechanisms underlying fibrosis, extracellular matrix densification, and chronic pain. Fasciae are interconnected connective tissue sheaths that maintain anatomical organization, allow tissue gliding, and facilitate mechanical force transmission between structures. Because of their mediating role in mechanical and biochemical signalling, fascial tissues are also involved in injury and regeneration processes. Pathological stiffening of fascial connections may impair regeneration by limiting mobility and disrupting mechanotransduction. Therefore, treatment strategies that target both muscle and fascial tissues may offer improved outcomes in the recovery of neuromusculoskeletal function.
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