Evidence map›Paper›PMID 42477143›Full record

ArticleActa pharmacologica Sinica2026

ATF3/SOX11-regulated FST activates IGF1R-ERK/AKT-Sp1 signaling to sustain trigeminal neuropathic pain.

Yue-Juan Ling, Bing Zhu, Zuo-Hao Yao, Ling-Jie Ma, Lin-Peng Zhu, Jing Zhang, Fei-Fei Xu, Hao Wu, Lu-Lu Ji, Yong-Jing Gao

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Acta pharmacologica Sinica, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing 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

1 citing paper in PubMed.

  1. Review
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

10 authors.

Yue-Juan Ling *Institute of Pain Medicine and Special Environmental Medicine, Co-Innovation Center of Neuroregeneration, Nantong University, Nantong, 226019, China.
Bing Zhu *Institute of Pain Medicine and Special Environmental Medicine, Co-Innovation Center of Neuroregeneration, Nantong University, Nantong, 226019, China.
Zuo-Hao Yao *Institute of Pain Medicine and Special Environmental Medicine, Co-Innovation Center of Neuroregeneration, Nantong University, Nantong, 226019, China.
Ling-Jie MaInstitute of Pain Medicine and Special Environmental Medicine, Co-Innovation Center of Neuroregeneration, Nantong University, Nantong, 226019, China.
Lin-Peng ZhuInstitute of Pain Medicine and Special Environmental Medicine, Co-Innovation Center of Neuroregeneration, Nantong University, Nantong, 226019, China.
Jing ZhangInstitute of Pain Medicine and Special Environmental Medicine, Co-Innovation Center of Neuroregeneration, Nantong University, Nantong, 226019, China.
Fei-Fei XuDepartment of Otolaryngology-Head Neck Surgery, The Second Affiliated Hospital of Nantong University, Nantong, 226019, China.
Hao WuDepartment of Otolaryngology-Head Neck Surgery, The Second Affiliated Hospital of Nantong University, Nantong, 226019, China.
Lu-Lu JiDepartment of Anesthesiology and Pain Management, The Affiliated Hospital of Nantong University, Nantong, 226001, China. baihelulu1@163.com.
Yong-Jing GaoInstitute of Pain Medicine and Special Environmental Medicine, Co-Innovation Center of Neuroregeneration, Nantong University, Nantong, 226019, China. gaoyongjing@ntu.edu.cn.ORCID http://orcid.org/0000-0002-7432-7458

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Trigeminal neuropathic pain (TNP) is a severe facial pain disorder whose pathogenesis is incompletely understood. We previously identified follistatin (FST) as a contributor to peripheral nerve injury-induced neuropathic pain through direct binding to the insulin-like growth factor-1 receptor (IGF1R) in the dorsal root ganglia. However, the regulatory mechanisms governing FST expression and its specific role in TNP remain unclear. Here, we report that FST is upregulated in trigeminal ganglion (TG) neurons following partial infraorbital nerve transection (pIONT), and that this process is regulated by the transcription factors ATF3 and SOX11. Genetic deletion or knockdown of Fst attenuated pIONT-induced TNP and reduced TG neuronal hyperexcitability. Intra-TG injection of FST promoted pain-like behaviors and activated ERK and AKT signaling in an IGF1R-dependent manner. In addition, FST decreased voltage-gated potassium (K

Indexed as

Activating Transcription Factor 3FollistatinNeuralgiaAnimalsExtracellular Signal-Regulated MAP KinasesMaleMiceProto-Oncogene Proteins c-aktReceptor, IGF Type 1Receptors, SomatomedinSignal TransductionSp1 Transcription FactorTrigeminal GanglionActivating Transcription Factor 3Atf3 protein, mouseExtracellular Signal-Regulated MAP KinasesFollistatinIgf1r protein, mouseProto-Oncogene Proteins c-aktReceptor, IGF Type 1Receptors, SomatomedinSp1 Transcription FactorAKTERKfollistatinIGF1RSp1trigeminal neuropathic pain

Identifiers

PMID42477143
PMCPMC13586176

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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.