ArticleNeuromolecular medicine2026
Transcription Factor SPI1 Mediates Chronic Neuropathic Pain by Activating NLRC4 Transcription to Drive Microglial Activation and Inflammation.
Article in Neuromolecular medicine, 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
4 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Microglial polarization plays a key role in the process of chronic neuropathic pain (CNP). This study aims to investigate the molecular mechanism by which the transcription factor SPI1 mediates microglial polarization and participates in CNP by regulating NOD-like receptor C4 (NLRC4) expression. The GSE124272 dataset (blood samples of 8 intervertebral disc degeneration patients and 8 controls) was obtained from the GEO database, and the differentially expressed genes (DEGs) were screened. The intersection of DEGs with neuropathic pain related genes in GeneCards was taken. Support vector machine-recursive feature elimination algorithm was used to identify hub genes. Human microglia (HMC3) were stimulated with lipopolysaccharides (LPS) to construct an inflammation model. qRT-PCR, western blot, ELISA, flow cytometry, and reactive oxygen species (ROS) detection were used to evaluate gene expression, inflammatory factor levels, cell polarization, and ROS levels. ChIP and dual-luciferase reporter assay were used to verify the binding of SPI1 to NLRC4 promoter and its transcriptional regulation. A rat model of chronic constriction injury (CCI) was established to evaluate the effect of shNLRC4 on CNP in vivo. After screening and machine learning, NLRC4 was one of the five hub genes, and its expression was significantly upregulated in LPS-induced HMC3 cells. NLRC4 knockdown inhibited LPS-induced M1 polarization, the release of pro-inflammatory factors, ROS production, and the expression of microglia activation marker Iba1, while promoted the expression of M2 polarization markers. SPI1 could directly bind to the NLRC4 promoter to increase its transcription. Overexpression of NLRC4 reversed the inhibitory effect of SPI1 knockdown on LPS-induced microglial activation and inflammation. In CCI rat model, knocking down NLRC4 significantly alleviated mechanical and thermal hyperalgesia, and reduced the levels of NLRC4 and inflammatory factors (TNF-α, IL-1β, and IL-6) in the spinal cord tissues. SPI1 acts as a transcription factor to directly increase NLRC4 transcription, thereby promoting microglial activation and neuroinflammatoion, and ultimately accelerating the development of CNP.
Indexed as
Identifiers
42096098What 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.