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.
Code
The paper links to its data and to no code of its authors: see the Data section.
Tracing map
A tracing map links a paper to the code its authors published: this paper has none, so it has no map.
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://
Reproduced under the paper's license (CC BY), from the paper cited above.
Versions
The history of this record: each version stored by the harvester or made by a correction of its authors or of the maintainers of its code, and what changed in its facts. The texts of the paper (its abstract, its availability statements) are not part of it; versions that changed only those are not listed.
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
{
"id": "10.1002/
"type": "article-journal",
"title": "VDAC1 Upregulation Induces Hyperexcitability of Nociceptive Sensory Neurons Via Enhanced Mitochondrial Atp Efflux in Neuropathic Pain",
"container-title": "Advanced science (Weinheim, Baden-Wurttemberg, Germany)",
"author": [
{
"family": "Sun",
"given": "Fengrun"
},
{
"family": "Yu",
"given": "Ning"
},
{
"family": "Yu",
"given": "Liang"
},
{
"family": "Tian",
"given": "Xiaofen"
},
{
"family": "Ma",
"given": "Yujia"
},
{
"family": "Xie",
"given": "Yikuan"
},
{
"family": "Wang",
"given": "Tao"
},
{
"family": "Ma",
"given": "Chao"
}
],
"container-title-short":
"page": "e23223",
"DOI": "10.1002/
"PMID": "42411405",
"PMCID": "PMC13339037",
"ISSN": "2198-3844",
"publisher": "Wiley",
"URL": "https://
"language": "en",
"issued": {
"date-parts": [
[
2026,
7,
7
]
]
}
}
Similar papers
The papers with a page that share the most with this one: the tools found in their code, their categories, datasets, cited references and authors, the rarest counting most.
- [1] doi:10.7554/elife.76063
- scRNA-sequencing reveals subtype-specific transcriptomic perturbations in DRG neurons of &
lt;i& gt;Pirt& lt;sup& gt;EGFPf& lt;/ sup& gt;& lt;/ i& gt; mice in neuropathic pain condition. Journal: eLifeIn common: NCBI GEO GSE216039, pain, cellular / molecular, 2 references - [2] doi:10.3390/ijms23179946
- Targeting the Mitochondrial Protein VDAC1 as a Potential Therapeutic Strategy in ALS.Journal: International journal of molecular sciencesIn common: cellular / molecular, 4 references
- [3] doi:10.1038/s41380-025-03250-3 [code]
- The China Brain Multi-omics Atlas Project (CBMAP).Journal: Molecular psychiatryIn common: author Chao Ma
- [4] doi:10.1038/s41467-024-46899-0
- The aldehyde dehydrogenase 2 rs671 variant enhances amyloid β pathology.Journal: Nature communicationsIn common: author Chao Ma
- [5] doi:10.1186/s40035-022-00329-7
- Targeting the overexpressed mitochondrial protein VDAC1 in a mouse model of Alzheimer's disease protects against mitochondrial dysfunction and mitigates brain pathology.Journal: Translational neurodegenerationIn common: cellular / molecular, 3 references
- [6] doi:10.1038/s41419-026-08445-2
- Time‑resolved multi-omic analysis of paclitaxel exposure in human iPSC‑derived sensory neurons unveils mechanisms of chemotherapy‑induced peripheral neuropathy.Journal: Cell death & diseaseIn common: pain, cellular / molecular, 2 references
- [7] doi:10.1038/s41467-025-62343-3
- Histone lactylation regulates DOCK4 to control heat nociception and supports Dynein-mediated Nav1.7 trafficking.Journal: Nature communicationsIn common: pain, cellular / molecular, 2 references
- [8] doi:10.1016/j.crmeth.2025.101051
- Profiling human iPSC-derived sensory neurons for analgesic drug screening using a multi-electrode array.Journal: Cell reports methodsIn common: pain, 2 references
- [9] doi:10.1016/j.celrep.2023.112295 [code]
- c-Maf-positive spinal cord neurons are critical elements of a dorsal horn circuit for mechanical hypersensitivity in neuropathy.Journal: Cell reportsIn common: pain, cellular / molecular, 2 references
- [10] doi:10.1016/j.stemcr.2026.102971
- A highly efficient method to differentiate CGRP-expressing peptidergic nociceptors from human induced pluripotent stem cells.Journal: Stem cell reportsIn common: pain, cellular / molecular, 2 references
Contribute
The authors of this paper can claim it, correct its record and validate its tracing map, and the maintainers of its code (its owner, or a public member of its organization) correct what it says of their repository; anyone signed in can ask for its removal. Every request goes to OSCR's own machine, which answers it; your account page follows them.
Sign in with ORCID to claim this paper as one of its authors, correct its record or validate its tracing map: when the paper's metadata lists your ORCID iD, you are recognized at once. Maintainers of its code: sign in with GitHub, then claim the repository on your account page.
Claim this paper
Correct its record
Say what each link of this record is, remove the ones that are not the paper's, add the ones that are missing. The correction becomes a new version of the record, in its Versions section.
Request its removal
To ask OSCR to remove this record, the copies of its authors' scripts or its tracing map, use the removal request page: signed in, you say who you are, what to remove and why, then review and confirm the request. Published rules decide every request (how).
Discussion, reproductions, activity
Discussion: code errors and mismatches between the code and the paper about this paper and its code, from readers and its authors, beside the paper and its tracing map.
Reproductions: reports from readers who ran the authors' code and did not get the paper's result, what they ran, with which environment, commit and data.
Activity: what happens around this paper: new versions of its record, its map's validation, discussions and reproductions. It opens with sign-in.