ArticleThe journal of headache and pain2023
BMP7 alleviates trigeminal neuralgia by reducing oligodendrocyte apoptosis and demyelination.
Article in The journal of headache and pain, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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10 citing papers in PubMed, 19 citations in OpenAlex.
- AAV Vector-Mediated Modulation of Signaling Pathways in Neurological Disorders: Insights From Cellular, Animal, and Human Studies.Cell biochemistry and function · 2026Review
- The Hypothesis of Myelinodegeneration as an Initial Risk of Neuropathic Pain.Neuroscience bulletin · 2026Review
- Identification and validation of candidate biomarkers associated with mitochondria and 18 types of programmed cell death in trigeminal neuralgia: insights from transcriptome sequencing.Frontiers in molecular neuroscience · 2026Article
- L3MBTL2 as a novel therapeutic target for trigeminal neuralgia: evidence from integrated TWAS, multi-tissue MR, and experimental validation.The journal of headache and pain · 2025Article
- Brown adipose tissue secretes OLFM4 to coordinate sensory and sympathetic innervation via Schwann cells.Nature communications · 2025Article
- Neuroplasticity and Nervous System Recovery: Cellular Mechanisms, Therapeutic Advances, and Future Prospects.Brain sciences · 2025Review
- DMH1-loaded peptide nanomicelles restore myelin and attenuate neuroinflammation in trigeminal neuralgia via CCL5 suppression.Frontiers in pharmacology · 2025Article
- Unraveling the role of oligodendrocytes and myelin in pain.Journal of neurochemistry · 2025Review
- Interleukin-22 receptor 1-mediated stimulation of T-type CaCell communication and signaling : CCS · 2024Article
- A non-toxic analgesic elicits cell-specific genomic and epigenomic modulation by targeting the PAG brain region.Neurobiology of pain (Cambridge, Mass.)Article
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Authors and funding
6 authors at 3 institutions in 2 countries.
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No grant is acknowledged in the PubMed record.
Abstract
backgroundBMP7 has been shown to have neuroprotective effects and to alleviate demyelination. However, its role in trigeminal neuralgia (TN) has not been well investigated. The current study aims to determine whether BMP7 plays a role in demyelination, its effects on pain behaviors and mechanism of action in rats with TN.
methodsWe used an infraorbital-nerve chronic-constriction injury (ION-CCI) to establish a rat model of TN. Adeno-associated viruses (AAVs) were injected into the rats to upregulate or downregulate BMP7. The mechanical withdrawal thresholds (MWT) of the injured rats were detected using Von Frey filaments. The changes in expression levels of BMP7 and oligodendrocyte (OL) markers were examined by western blotting, quantitative real-time PCR, immunofluorescence, and transmission electron microscopy.
resultsThe ION-CCI induced mechanical allodynia, demyelination, and loss of OLs with a reduction of BMP7. Short-hairpin RNA (shRNA)-BMP7 that inhibited BMP7 expression also caused mechanical allodynia, demyelination, and loss of OLs, and its mechanism may be OL apoptosis. Overexpressing BMP7 in the trigeminal spinal subnucleus caudalis(VC) with AAV-BMP7 relieved all three phenotypes induced by the CCI, and its mechanism may be alleviating OLs apoptosis. Two signal pathways associated with apoptosis, STAT3 and p65, were significantly downregulated in the VC after CCI and rescued by BMP7 overexpression.
conclusionBMP7 can alleviate TN by reducing OLs apoptosis and subsequent demyelination. The mechanism behind this protection could be BMP7-mediated activation of the STAT3 and NF-κB/p65 signaling pathway and subsequent decrease in OL apoptosis. Importantly, our study presents clear evidence in support of BMP7 as a possible therapeutic target for the treatment of TN.
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