ArticleCNS neuroscience & therapeutics2026
Recombinant Artemin-Fc Fusion Protein Attenuates TLR4/NF-κB-Associated Neuroinflammation and Modulates Inhibitory/Excitatory Synaptic Marker Expression After Spinal Cord Injury.
Article in CNS neuroscience & therapeutics, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors.
Funding
Abstract
aimsSpinal cord injury (SCI) can cause severe neurological dysfunction and the occurrence of chronic neuropathic pain, which can manifest as the occurrence of abnormal pain and hyperalgesia. Artemin (ARTN) is a member of the glial cell-derived neurotrophic factor (GDNF) family ligand and can improve neural injury and regulate the occurrence of neuropathic pain. However, the process by which ARTN regulates inflammation and the sensitization of the dorsal horn of the spinal cord related to pain after SCI is still unclear.
methodsARTN-Fc fusion protein was constructed and administered intrathecally to mice after SCI. Motor recovery and pain-related behaviors were evaluated using behavioral, gait, electrophysiological, paw withdrawal latency, and formalin-induced Fos assays. Molecular changes were assessed by Western blotting, immunofluorescence, and immunohistochemistry. In vitro, a BV2-PC12 Transwell co-culture system was used to examine the effect of ARTN-Fc on activated microglia-mediated neuronal injury.
resultsARTN-Fc treatment significantly improved motor recovery and reduced thermal hyperalgesia after SCI. Mechanistically, ARTN-Fc promoted microglial M2 polarization, inhibited TLR4/NF-κB activation, suppressed pro-inflammatory cytokine expression, and attenuated NLRP3 inflammasome/pyroptosis-related signaling. In the spinal dorsal horn, ARTN-Fc increased inhibitory GABAergic markers, including vGAT and GAD1, while reducing the excitatory marker vGluT2, suggesting altered inhibitory/excitatory synaptic marker expression. In vitro, ARTN-Fc reduced neuronal apoptosis mediated by activated microglia.
conclusionTaken together, the results suggest that ARTN-Fc is a potential therapeutic agent for SCI repair and neuropathic pain treatment by inhibiting the TLR4/NF-κB pathway to suppress neuroinflammation and modulating inhibitory/excitatory synaptic marker expression in the spinal dorsal horn.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.