Evidence map›Paper›PMID 41990262›Full record

ArticleAdvanced science (Weinheim, Baden-Wurttemberg, Germany)2026

Targeting the PDK1/c-Myc/SOX10 Signaling in Oligodendrocytes Alleviates Neuropathic Pain.

Pingping Qiao, Lifang Guo, Guochao Yang, Chaoli Huang, He Wang, Jian-Jun Yang, Guiquan Chen, Yimin Hu

Abstract read
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In one paragraph

Article in Advanced science (Weinheim, Baden-Wurttemberg, Germany), 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

8 authors.

Pingping QiaoState Key Laboratory of Pharmaceutical Biotechnology, Department of Neurosurgery, Nanjing Drum Tower Hospital, Affiliated Hospital of Medical School, Jiangsu Key Laboratory of Molecular Medicine, Model Animal Research Center, Medical School, Nanjing University, Nanjing, China.ORCID https://orcid.org/0000-0002-4270-9670
Lifang GuoDepartment of Laser Surgery, Hospital of Dermatology, Chinese Academy of Medical Sciences and Peking Union Medical College, Nanjing, China.
Guochao YangState Key Laboratory of Pharmaceutical Biotechnology, Department of Neurosurgery, Nanjing Drum Tower Hospital, Affiliated Hospital of Medical School, Jiangsu Key Laboratory of Molecular Medicine, Model Animal Research Center, Medical School, Nanjing University, Nanjing, China.
Chaoli HuangDepartment of Anesthesiology and Perioperative Medicine, The First Affiliated Hospital of Nanjing Medical University, Nanjing, China.ORCID https://orcid.org/0000-0003-1411-1417
He WangDepartment of Anesthesiology, Pain and Perioperative Medicine, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, China.
Jian-Jun YangDepartment of Anesthesiology, Pain and Perioperative Medicine, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, China.ORCID https://orcid.org/0000-0001-6785-9627
Guiquan ChenState Key Laboratory of Pharmaceutical Biotechnology, Department of Neurosurgery, Nanjing Drum Tower Hospital, Affiliated Hospital of Medical School, Jiangsu Key Laboratory of Molecular Medicine, Model Animal Research Center, Medical School, Nanjing University, Nanjing, China.ORCID https://orcid.org/0000-0002-4674-5548
Yimin HuDepartment of Anesthesiology, Hospital of Dermatology, Chinese Academy of Medical Sciences and Peking Union Medical College, Nanjing, China.

Funding

Key Medical Projects from Jiangsu Provincial Health Commission K2025040National Natural Science Foundation of China 32270871National Natural Science Foundation of China 82201330National Natural Science Foundation of China U23A20421
6 · The paper itself

Abstract

Neuropathic pain (NPP) is a critical clinical challenge with limited therapeutic options. While neuronal mechanisms have been extensively studied, the contribution of oligodendrocyte (OL) homeostasis to NPP pathogenesis is poorly understood. Here, we show that chronic constriction injury (CCI) causes demyelination and downregulation of 3-phosphoinositide-dependent kinase 1 (PDK1) in the central nervous system (CNS) in mice. Functional analysis of inducible OL lineage-specific Pdk1 conditional knockout (Pdk1 cKO) mice reveals mechanical allodynia and thermal hyperalgesia, a pattern of sensory changes that closely resembles NPP in CCI mice. RNA sequencing (RNA-seq), morphological, and molecular analyses demonstrate that PDK1 deficiency impairs myelination via the c-Myc/SOX10 axis. Notably, pharmacological enhancement of remyelination or AAV-mediated knockdown of c-Myc restores nodal integrity and alleviates NPP in Pdk1 cKO mice. Our findings establish PDK1-mediated OL homeostasis as a critical determinant of NPP pathogenesis and identify c-Myc modulation as a novel therapeutic strategy for NPP.

Indexed as

3-Phosphoinositide-Dependent Protein KinasesNeuralgiaOligodendrogliaProto-Oncogene Proteins c-mycSOXE Transcription FactorsAnimalsDisease Models, AnimalMaleMiceMice, KnockoutPyruvate Dehydrogenase Acetyl-Transferring KinaseSignal Transduction3-Phosphoinositide-Dependent Protein KinasesMyc protein, mousePdk1 protein, mouseProto-Oncogene Proteins c-mycPyruvate Dehydrogenase Acetyl-Transferring KinaseSOXE Transcription Factorsc‐Mycmyelinneuropathic painoligodendrocytePDK1SOX10

Identifiers

PMID41990262
PMCPMC13334879

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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.