Related Experiment Video
Updated: Dec 24, 2025
Temporomandibular Joint Pain Measurement by Bite Force and Von Frey Filament Assays in Mice
Published on: September 13, 2024
Peripheral FGFR1 Regulates Myofascial Pain in Rats via the PI3K/AKT Pathway
Mingyang Zhang1, Feihong Jin2, Yuchang Zhu3
1Department of Anesthesiology and Pain Clinic, Qilu Hospital of Shandong University, 107 Wenhuaxi Road, Ji'nan, Shandong 250012, China; Department of Anesthesiology, Tengzhou Central People's Hospital, 181 Xingtan Road, Tengzhou, Shandong 277500, China.
Abstract:
Myofascial pain syndrome (MPS) is a type of skeletal pain identified by myofascial trigger points (MTrPs). The formation of MTrPs is linked to muscle damage. The fibroblast growth factor receptor (FGFR1) has been found to cause pain sensitivity while repairing tissue damage. The aim of the current study was to explore the mechanism of FGFR1 in MTrPs. We used a RayBio human phosphorylation array kit to measure p-FGFR1 levels in human control subjects and patients with MTrPs. P-FGFR1 was upregulated in the patients with MTrPs. Then a rat model of MPS was established by a blunt strike on the left gastrocnemius muscles (GM) and eccentric-exercise for 8 weeks with 4 weeks of recovery. After establishing the MPS model, the morphology of the GM changed, and the differently augmented sizes of round fibers (contracture knots) in the transverse section and fusiform shapes in the longitudinal section were clearly seen in the rats with myofascial pain. The expression of p-FGFR1 was upregulated on the peripheral nerves and dorsal root ganglion neurons in the MTrPs group. The spinal Fos protein expression was increased in the MTrPs group. Additionally, the mechanical pain threshold was reduced, and the expression of FGF2, p-FGFR1, PI3K-p110γ, and p-AKT increased in the MTrPs group. PD173074 increased the mechanical pain threshold of the MTrPs group, and inhibited the expression of p-FGFR1, PI3K-p110γ, and p-AKT. Moreover, LY294002 increased the mechanical pain threshold of the MTrPs group. These findings suggest that FGFR1 may regulate myofascial pain in rats through the PI3K/AKT pathway.
Insights
Fibroblast growth factor receptor 1 (FGFR1) is upregulated in myofascial pain syndrome (MPS). Targeting FGFR1 with PD173074 or LY294002 may alleviate pain by inhibiting the PI3K/AKT pathway.
Area of Science:
- Biomedical research
- Pain management
- Molecular biology
Background:
- Myofascial pain syndrome (MPS) is characterized by myofascial trigger points (MTrPs) linked to muscle damage.
- Fibroblast growth factor receptor 1 (FGFR1) plays a role in pain sensitivity during tissue repair.
- The precise mechanism of FGFR1 in MTrPs requires further investigation.
Purpose of the Study:
- To explore the role and mechanism of FGFR1 in the development of myofascial trigger points (MTrPs).
- To investigate the involvement of the PI3K/AKT pathway in FGFR1-mediated myofascial pain.
Main Methods:
- Measured phosphorylated FGFR1 (p-FGFR1) levels in human MPS patients and controls using a phosphorylation array.
- Established a rat model of MPS via blunt strike and eccentric exercise, followed by morphological and molecular analysis.
- Assessed p-FGFR1 expression in peripheral nerves and dorsal root ganglion neurons, spinal Fos protein, and mechanical pain thresholds.
Main Results:
- p-FGFR1 was upregulated in human MPS patients and in the rat MPS model, particularly on peripheral nerves and dorsal root ganglion neurons.
- MPS rats showed reduced mechanical pain thresholds and increased expression of FGF2, p-FGFR1, PI3K-p110γ, and p-AKT.
- Inhibition of FGFR1 (PD173074) or PI3K (LY294002) pathways increased mechanical pain thresholds in MPS rats.
Conclusions:
- FGFR1 signaling is upregulated in myofascial pain syndrome.
- FGFR1 appears to regulate myofascial pain in rats, potentially through activation of the PI3K/AKT pathway.
- Targeting FGFR1 may offer a therapeutic strategy for managing myofascial pain.
