Evidence map›Paper›PMID 41957340›Full record

ArticleNeuroscience bulletin2026

Targeting Fgr-STAT3 Mediated Autophagy Inhibition in the Spinal Cord Alleviates Neuropathic Pain in Rats.

Liqiong He, Yu Zhang, Chunguang Yang, Zhifeng Huang, Kailu Zou, Qingwei Deng, Jianxi Zhang, Malijiang Mulati, Bei Sun, Qulian Guo and 1 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Neuroscience bulletin, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
–field-weighted citation impact
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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

11 authors.

Liqiong HeDepartment of Anesthesiology, Xiangya Hospital, Central South University, Changsha, 410000, China.
Yu ZhangDepartment of Anesthesiology, Fujian Medical University Union Hospital, Fuzhou, 350000, China.
Chunguang YangDepartment of Anesthesiology, Xiangya Hospital, Central South University, Changsha, 410000, China.
Zhifeng HuangDepartment of Anesthesiology, Xiangya Hospital, Central South University, Changsha, 410000, China.
Kailu ZouDepartment of Anesthesiology, Xiangya Hospital, Central South University, Changsha, 410000, China.
Qingwei DengDepartment of Anesthesiology, Xiangya Hospital, Central South University, Changsha, 410000, China.
Jianxi ZhangDepartment of Anesthesiology, Xiangya Hospital, Central South University, Changsha, 410000, China.
Malijiang MulatiDepartment of Anesthesiology, Xiangya Hospital, Central South University, Changsha, 410000, China.
Bei SunDepartment of Anesthesiology, Xiangya Hospital, Central South University, Changsha, 410000, China.
Qulian GuoDepartment of Anesthesiology, Xiangya Hospital, Central South University, Changsha, 410000, China.
Changsheng HuangDepartment of Anesthesiology, Xiangya Hospital, Central South University, Changsha, 410000, China. changsheng.huang@csu.edu.cn.ORCID http://orcid.org/0000-0003-0535-1865

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The effective treatment of neuropathic pain continues to be a major clinical hurdle, largely because its pathogenic mechanisms are incompletely defined. This study identifies Fgr kinase as a central player in governing autophagy within spinal microglia during the development of neuropathic pain. Using a rat model of chronic constriction injury (CCI), we found that damage to peripheral nerves causes a prolonged increase in Fgr expression specifically in microglia of the spinal dorsal horn (SDH). Genetic interventions and behavioral analyses demonstrated that Fgr overexpression induced pain symptoms, whereas Fgr knockdown alleviated pain hypersensitivity. Mechanistically, Fgr directly phosphorylated STAT3, promoting its nuclear translocation and suppressing autophagic flux, evidenced by reduced LC3-II/LC3-I ratio, accumulated SQSTM1, and diminished autophagosomes. Pharmacological inhibition of Fgr by intrathecal TL02-59 (10 μg/kg) restored autophagy, attenuated STAT3 activation, and reversed CCI-induced neuropathic pain behaviors. These findings position the Fgr-STAT3 axis as a tractable target to normalize microglial autophagy and alleviate neuropathic pain.

Indexed as

AutophagyNeuralgiaSpinal CordSTAT3 Transcription FactorAnimalsDisease Models, AnimalHyperalgesiaMaleMicrogliaPhosphorylationRatsRats, Sprague-DawleyStat3 protein, ratSTAT3 Transcription FactorAutophagyFgr kinaseMicrogliaNeuropathic painSTAT3 phosphorylation

Identifiers

PMID41957340
PMCPMC13545190

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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.