ArticleMolecular pain2022
Targeting Vascular endothelial growth factor A with soluble vascular endothelial growth factor receptor 1 ameliorates nerve injury-induced neuropathic pain.
Article in Molecular pain, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 11 citations in OpenAlex.
- Review
- Dihydromyricetin Modulates Neuropathic Pain and Depression: A Correlation with Hippocampal Vascular Endothelial Growth Factor in Mice.Journal of inflammation research · 2026Article
- Development of a High-throughput Morphological Assay for Evaluating Mesenchymal Stromal Cell-derived Extracellular Vesicle Modulation of Brain Pericyte Secretory Phenotype.Stem cell reviews and reports · 2025Article
- Vascular Endothelial Growth Factor a Promotes Chronic Itch via VEGFA-VEGFR2-PI3K-TRPV1 Axis in Allergic Contact Dermatitis.Journal of inflammation research · 2024Article
- Ac4C Enhances the Translation Efficiency of Vegfa mRNA and Mediates Central Sensitization in Spinal Dorsal Horn in Neuropathic Pain.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2023Article
- Mechanism of gene network in the treatment of intracerebral hemorrhage by natural plant drugs in Lutong granules.PloS one · 2022Article
- Network Pharmacology-Based Dissection of the Mechanism of Drynariae Rhizoma for Low Back Pain.BioMed research international · 2022Article
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Neuropathic pain is a distressing medical condition with few effective treatments. The role of Vascular endothelial growth factor A (VEGFA) in inflammation pain has been confirmed in many researches. However, the mechanism of VEGFA affects neuropathic pain remains unclear. In this study, we demonstrated that VEGFA plays an important role in spare nerve injury (SNI)-induced neuropathic pain, which is mediated by enhanced expression and colocalized of VEGFA, p-AKT and TRPV1 in SNI-induced neuropathic pain model. Soluble VEGFR1 (sFlt1) not only relieved mechanical hyperalgesia and the expression of inflammatory markers, but ameliorated the expression of VEGFA, VEGFR2, p-AKT, and TRPV1 in spinal cord. However, these effects of sFlt1 can be blocked by rpVEGFA and by 740 Y-P. Therefore, our study indication that targeting VEGFA with sFlt1 reduces neuropathic pain development via the AKT/TRPV1 pathway in SNI-induced nerve injury. This study elucidates a new therapeutic target for neuropathic pain.
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