VDAC1 Upregulation Induces Hyperexcitability of Nociceptive Sensory Neurons Via Enhanced Mitochondrial Atp Efflux in Neuropathic Pain.
Overview
- State Key Laboratory of Common Mechanism Research for Major Diseases, Department of Human Anatomy, Histology and Embryology, Neuroscience Center, Joint Laboratory of Anesthesia and Pain, Institute of Basic Medical Sciences Chinese Academy of Medical Sciences, School of Basic Medicine Peking Union Medical College, Beijing, China
- Department of Anatomy, Key Laboratory of Human Brain Bank for Functions and Diseases of Department of Education of Guizhou Province, Guizhou Medical University, Guiyang, Guizhou, China
- National Human Brain Bank for Development and Function, Beijing, China
- Chinese Institute for Brain Research, Beijing, China
Abstract
Neuropathic pain results from aberrant sensory processing following nerve injury. Voltage‐dependent anion channels (VDACs), a family of ATP gatekeepers in the outer mitochondrial membrane, are central to cellular metabolism and action potential generation, yet their roles in peripheral neuropathic pain remain poorly defined. Here, we demonstrate that among the VDAC isoforms, VDAC1 is predominantly expressed in dorsal root ganglion (DRG) nociceptive neurons and is markedly upregulated in a mouse model of chronic constriction injury (CCI). Functionally, VDAC1 promotes neuropathic pain by increasing mitochondrial ATP permeability, thereby elevating cytoplasmic ATP levels and enhancing neuronal excitability. Genetic or pharmacological inhibition of VDAC1 reduced cytoplasmic ATP, suppresses neuronal hyperexcitability, and alleviates pain behaviors. Collectively, these findings indicate the role of VDAC1 in ATP dynamics and neuronal excitability, highlighting it as a potential therapeutic target for neuropathic pain.
Reproduced under the paper's license (CC BY), from the paper cited above.
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Data
Datasets cited
- geo:GSE216039 — at NCBI GEO; found in the text, “Bioinformatic Analysis”
Data Availability Statement
The data that supports the findings of this study are available from the corresponding author upon reasonable request. For bioinformatic analysis, scRNA‐seq of mice from Sham and CCI 7 d groups were obtained from GEO accession #GSE216039 (https://
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Version 1, 27 September 2026: the first record
Recorded: type, language, journal, pages, dates, 8 authors, 5 keywords, 1 funder, 70 references.
Cite
This paper
Sun, F., Yu, N., Yu, L., Tian, X., Ma, Y., Xie, Y., Wang, T., & Ma, C. (2026). VDAC1 Upregulation Induces Hyperexcitability of Nociceptive Sensory Neurons Via Enhanced Mitochondrial Atp Efflux in Neuropathic Pain. Advanced science (Weinheim, Baden-Wurttemberg, Germany), e23223. https://
BibTeX
@article{sun2026vdac1,
author = {Sun, Fengrun and Yu, Ning and Yu, Liang and Tian, Xiaofen and Ma, Yujia and Xie, Yikuan and Wang, Tao and Ma, Chao},
title = {{VDAC1 Upregulation Induces Hyperexcitability of Nociceptive Sensory Neurons Via Enhanced Mitochondrial Atp Efflux in Neuropathic Pain}},
journal = {Advanced science (Weinheim, Baden-Wurttemberg, Germany)},
year = {2026},
month = jul,
pages = {e23223},
publisher = {Wiley},
issn = {2198-3844},
doi = {10.1002/
url = {https://
pmid = {42411405},
pmcid = {PMC13339037}
}
RIS
TY - JOUR
AU - Sun, Fengrun
AU - Yu, Ning
AU - Yu, Liang
AU - Tian, Xiaofen
AU - Ma, Yujia
AU - Xie, Yikuan
AU - Wang, Tao
AU - Ma, Chao
TI - VDAC1 Upregulation Induces Hyperexcitability of Nociceptive Sensory Neurons Via Enhanced Mitochondrial Atp Efflux in Neuropathic Pain
T2 - Advanced science (Weinheim, Baden-Wurttemberg, Germany)
J2 - Adv Sci (Weinh)
PY - 2026
DA - 2026/
SP - e23223
SN - 2198-3844
PB - Wiley
DO - 10.1002/
UR - https://
LA - en
ER -
CSL-JSON
{
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"container-title": "Advanced science (Weinheim, Baden-Wurttemberg, Germany)",
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