Immune Cells May Hold the Key to Fighting Obesity-Induced Muscle Dysfunction
Summary
Researchers reveal how deleting a key signaling molecule from a subpopulation of macrophages enhances muscle regeneration and mitochondrial function
Obesity has been linked to skeletal muscle loss and deterioration. While M2 macrophages may play a role in regulating muscle function, the underlying mechanisms remain poorly understood. Now, researchers from Japan have found that deleting the signaling protein transforming growth factor-beta 1 from a specific population of M2 macrophages protected mice from obesity-induced muscle dysfunction. This enhanced muscle regeneration and mitochondrial function, suggesting a potential therapeutic strategy for muscle loss associated with obesity.
- Image title： Toward effective therapeutic strategies for obesity-related sarcopenia
- Image caption： This study clarifies the role of a specific population of immune cells in the deterioration of muscle tissue in the context of obesity. Targeting transforming growth factor-beta 1 (TGF-β1) signaling in CD206+ M2 macrophages could represent a promising strategy for counteracting obesity-related muscle loss by enhancing muscle regeneration and improving mitochondrial function.
- Credit：Distinguished Research Professor Kazuyuki Tobe from the University of Toyama
- License type：Original content
- Usage restrictions：Cannot be reused without permission.
Research Details
Immune Cells May Hold the Key to Fighting Obesity-Induced Muscle Dysfunction[PDF, 496KB]
Reference
Title of original paper
Deletion of Tgf-β1 From CD206+ M2 Macrophages Ameliorates Obesity-Induced Suppression of Myogenesis and AMPK Phosphorylation in Skeletal Muscle
Journal
Journal of Cachexia, Sarcopenia and Muscle
DOI
https://doi.org/10.1002/jcsm.70322
Additional information for EurekAlert
Latest Article Publication Date
18 June, 2026
Method of Research
Experimental study
Subject of Research
Animals
Conflicts of Interest Statement
The authors declare no conflicts of interest.
Media contact
Yumiko Kato
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