Evidence map›Paper›PMID 41321642›Full record

ArticleiScience2025

Astrocyte-to-neuron interaction via NF-κB/C3/C3aR mediates chronic post-thoracotomy pain by modulating neuronal GluR1 in spinal dorsal horn.

Wanying Mou, Ning Yu, Fengrun Sun, Huan Cui, Hanyu Zhang, Yan Cao, Sixuan Jin, Chao Ma, Afang Zhu, Lulu Ma and 1 more

Abstract read
In one paragraph

Article in iScience, 2025. 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.

Wanying MouDepartment of Anesthesiology, Peking Union Medical College Hospital, Chinese Academy of Medical Sciences & Peking Union Medical College, Beijing, China.
Ning YuState Key Laboratory of Common Mechanism Research for Major Diseases, Department of Human Anatomy, Histology and Embryology, Neuroscience Center, Institute of Basic Medical Sciences, Chinese Academy of Medical Sciences, School of Basic Medicine, Peking Union Medical College, Beijing, China.
Fengrun SunState Key Laboratory of Common Mechanism Research for Major Diseases, Department of Human Anatomy, Histology and Embryology, Neuroscience Center, Institute of Basic Medical Sciences, Chinese Academy of Medical Sciences, School of Basic Medicine, Peking Union Medical College, Beijing, China.
Huan CuiState Key Laboratory of Common Mechanism Research for Major Diseases, Department of Human Anatomy, Histology and Embryology, Neuroscience Center, Institute of Basic Medical Sciences, Chinese Academy of Medical Sciences, School of Basic Medicine, Peking Union Medical College, Beijing, China.
Hanyu ZhangDepartment of General Surgery, Peking Union Medical College Hospital, Peking Union Medical College & Chinese Academy of Medical Sciences, Beijing, China.
Yan CaoState Key Laboratory of Common Mechanism Research for Major Diseases, Department of Human Anatomy, Histology and Embryology, Neuroscience Center, Institute of Basic Medical Sciences, Chinese Academy of Medical Sciences, School of Basic Medicine, Peking Union Medical College, Beijing, China.
Sixuan JinState Key Laboratory of Common Mechanism Research for Major Diseases, Department of Human Anatomy, Histology and Embryology, Neuroscience Center, Institute of Basic Medical Sciences, Chinese Academy of Medical Sciences, School of Basic Medicine, Peking Union Medical College, Beijing, China.
Chao MaState Key Laboratory of Common Mechanism Research for Major Diseases, Department of Human Anatomy, Histology and Embryology, Neuroscience Center, Institute of Basic Medical Sciences, Chinese Academy of Medical Sciences, School of Basic Medicine, Peking Union Medical College, Beijing, China.
Afang ZhuDepartment of Anesthesiology, Peking Union Medical College Hospital, Chinese Academy of Medical Sciences & Peking Union Medical College, Beijing, China.
Lulu MaDepartment of Anesthesiology, Peking Union Medical College Hospital, Chinese Academy of Medical Sciences & Peking Union Medical College, Beijing, China.
Yuguang HuangDepartment of Anesthesiology, Peking Union Medical College Hospital, Chinese Academy of Medical Sciences & Peking Union Medical College, Beijing, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Chronic post-thoracotomy pain (CPTP) is a debilitating postoperative complication associated with persistent hypersensitivity and neuroinflammatory changes. Here, we identify an astrocyte-neuron signaling cascade mediated by NF-κB/C3/C3aR that drives excitatory synaptic remodeling in the spinal dorsal horn during CPTP. Using a rat model, we show that the activation of astroglial NF-κB promotes C3 synthesis, which interacts with neuronal C3aR to enhance GluR1 expression and synaptic localization, thereby facilitating pain hypersensitivity. The pharmacological inhibition of NF-κB or knockdown of astroglial C3 or neuronal C3aR markedly attenuated mechanical and cold allodynia, accompanied by reduced GluR1 expression. These findings define a mechanistic link between glial NF-κB activation, complement signaling, and neuronal excitatory transmission, highlighting the NF-κB/C3/C3aR pathway as a potential therapeutic target for chronic postoperative pain.

Indexed as

Biological sciencesCell biologyNatural sciencesNeuroscience

Identifiers

PMID41321642
PMCPMC12664382

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Registered trials

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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.