Relationship between muscle FNDC5, FGF21 mRNA, miR-150 and bone loss after sciatic denervation
Teresa Priego1, Elena Nebot-Valenzuela2, Álvaro Moreno-Rupérez3
1Departamento de Fisiología, Facultad de Enfermería, Fisioterapia y Podología, Universidad Complutense de Madrid, Madrid, Spain.
Journal of Physiology and Biochemistry
|July 4, 2026
Summary
Muscle atrophy from sciatic denervation impacts bone density. Specific myokines like FGF21, FNDC5, and miR-150, but not IL-6 or IGF-1, appear to mediate this muscle-bone crosstalk and bone loss.
Area of Science:
- Muscle physiology
- Bone biology
- Endocrinology
Background:
- Muscle influences bone physiology, but mechanisms are unclear.
- Sciatic denervation in rats causes muscle atrophy and osteoporosis.
- Understanding muscle-bone crosstalk is crucial for treating bone loss.
Purpose of the Study:
- To investigate myokine expression in atrophic soleus muscle.
- To determine the effect of muscle atrophy on tibia microarchitecture.
- To explore the role of specific myokines in mediating muscle-bone interactions.
Main Methods:
- Sciatic denervation model in male rats (9-12 weeks old).
- Real-time PCR to measure soleus mRNA and microRNA expression (IGF-1, IL-6, FNDC5, FGF21, miR-150).
- Micro-computed tomography to assess tibia microarchitecture at 3, 7, and 14 days post-denervation.
Main Results:
- Denervation caused soleus atrophy and decreased tibia bone density, thickness, and number.
- Atrophic soleus showed increased IL-6, IGF-1, FGF21 mRNA, and decreased FNDC5 mRNA and miR-150.
- FGF21 negatively correlated with bone mineral content; FNDC5 and miR-150 positively correlated with bone parameters.
Conclusions:
- Muscle atrophy significantly alters tibia microarchitecture.
- FGF21, FNDC5, and miR-150 are implicated in muscle-bone crosstalk during atrophy.
- IL-6 and IGF-1 do not appear to be primary mediators of bone loss in this model.
