Evidence map›Paper›PMID 37622691›Full record

ArticleCurrent molecular medicine2024

Mechanism of IRF5-regulated CXCL13/CXCR5 Signaling Axis in CCI-induced Neuropathic Pain in Rats.

Jiawei Cao, Chungu Hu, Zhuofeng Ding, Juan Chen, Songhua Liu, Qiongcan Li

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Article in Current molecular medicine, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
0.7field-weighted citation impact, top 30% of its field
1 · What the graph read from it

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

3 citing papers in PubMed, 4 citations in OpenAlex.

  1. CXCL13/CXCR5: a new target for pain treatment.International journal of surgery (London, England) · 2025
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

6 authors at 2 institutions in 1 country.

Jiawei CaoDepartment of Anesthesiology, Changsha Central Hospital Affiliated to South China University, Changsha, 410028, Hunan, China.
Chungu HuDepartment of Anesthesiology, Changsha Central Hospital Affiliated to South China University, Changsha, 410028, Hunan, China.
Zhuofeng DingDepartment of Anesthesiology, Xiangya Hospital, Central South University, Changsha, 410008, Hunan, China.
Juan ChenDepartment of Anesthesiology, Changsha Central Hospital Affiliated to South China University, Changsha, 410028, Hunan, China.
Songhua LiuDepartment of Anesthesiology, Changsha Central Hospital Affiliated to South China University, Changsha, 410028, Hunan, China.
Qiongcan LiDepartment of Anesthesiology, Changsha Central Hospital Affiliated to South China University, Changsha, 410028, Hunan, China.
Central South University · CNChangsha Central Hospital · CN

Funding

Changsha Municipal Natural Science Foundation kq2014022National Natural Science Foundation of China 81901143
6 · The paper itself

Abstract

backgroundNeuropathic pain is chronic and affects the patient's life. Studies have shown that IRF5 and CXCL13/CXCR5 are involved in neuropathic pain; however, their interactions are unknown.

objectiveIn this study, a rat neuropathic pain model was constructed by inducing chronic compression injury (CCI). IRF5 recombinant lentiviral vector and CXCL13 neutralizing antibody were administered to investigate their action mechanisms in neuropathic pain. Consequently, the new strategies for disease treatment could be evolved.

methodsThe CCI rats were intrathecally injected with recombinant lentivirus plasmid LV-IRF5 (overexpression), LV-SH-IRF5 (silencing), and CXCL13 neutralizing antibody. Mechanical withdrawal threshold (MWT) and thermal withdrawal latency (TWL) were measured. The tumor necrosis factor (TNF)-alpha, interleukin (IL)-1β, and IL-6 levels were recorded via the enzyme-linked immunosorbent assay (ELISA). The spinal cord was stained using hematoxylin-eosin (HE). The binding of IRF5 to CXCL13 was analyzed by chromatin immunoprecipitation (ChIP) and dual luciferase reporter assay. The IRF5, neuronal nuclei (NeuN), CXCL13, and CXCR5 expressions were detected through quantitative real-time polymerase chain reaction and Western blot.

resultsThe MWT and TWL values in the CCI group were lower than in the Sham group. The expressions of CXCL13, CXCR5, and IRF5 in CCI rats were gradually increased with the modeling time. IRF5 silencing suppressed the expression of NeuN and lumbar enlargement in CCI rats and promoted MWT and TWL. Moreover, IRF5 silencing inhibited the expressions of CXCR5 and CXCL13 genes and down-regulated the expression levels of inflammatory factors. IRF5 was directly and specifically bound with the endogenous CXCL13 promoter and thus regulated it. IRF5 overexpression exacerbated the disease phenotype of CCI-induced neuropathic pain in rats. Administration of CXCL13 neutralizing antibodies reversed the IRF5 overexpression effects.

conclusionThe IRF5 silencing alleviated neuropathic pain in CCI rats by downregulating the pain threshold, inflammatory cytokine levels, and CXCL13/CXCR5 signaling. IRF5 overexpression exacerbated the disease parameters of CCI-induced neuropathic pain in rats; however, they were reversed by neutralizing antibodies against CXCL13.

Indexed as

Chemokine CXCL13Interferon Regulatory FactorsNeuralgiaReceptors, CXCR5Signal TransductionAnimalsDisease Models, AnimalMaleRatsRats, Sprague-DawleyChemokine CXCL13Cxcr5 protein, ratInterferon Regulatory FactorsIRF5 protein, ratReceptors, CXCR5CCIchronic compression injury.CXCL13CXCR5IRF5neuropathic pain

Identifiers

PMID37622691
OpenAlexW4386153584

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Registered trials

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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.