ArticleMediators of inflammation2023
TMEM100 Regulates Neuropathic Pain by Reducing the Expression of Inflammatory Factors.
Article in Mediators of inflammation, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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3 citing papers in PubMed, 6 citations in OpenAlex.
- Repetitive transcranial magnetic stimulation modulates neuroinflammation and cell apoptosis via the interaction between Ifit3 and Stat1 for the treatment of neuropathic pain.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026Article
- A novel clip-based nerve compression model with high stability and reproducibility for the study of chronic nerve injury associated with neuropathic pain.Frontiers in neuroscience · 2026Article
- TMEM100 Regulates Neuropathic Pain by Reducing the Expression of Inflammatory Factors.Mediators of inflammation · 2023Article
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Authors and funding
11 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
There is no effective treatment for peripheral nerve injury-induced chronic neuropathic pain (NP), which profoundly impacts the quality of life of those affected. Transmembraneprotein100 (TMEM100) is considered to be a pain regulatory protein and is expressed in the dorsal root ganglion (DRG) of rats. However, the mechanism of pain regulation and the expression of TMEM100 following various peripheral nerve injuries are unclear. In this study, we constructed two pain models of peripheral nerve injury: tibial nerve injury (TNI) and chronic constriction injury (CCI). This study found that the Paw Withdrawal Mechanical Threshold (PWMT) and Paw Withdraw Thermal Latency (PWTL) of the rats in the two pain models decreased significantly, and the expression of TMEM100 in the DRG of two groups also decreased significantly. Furthermore, the decrease in the CCI group was more obvious than in the TNI group. There was no significant statistical significance (
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