Evidence map›Paper›PMID 42343442›Full record

ArticleJournal of neuroinflammation2026

Complement C5a/C5aR1 pathway facilitates glioblastoma progression via fostering glioma stem cell-macrophage symbiosis.

Hongtao Zhu, Lidong Cheng, Dan Liu, Yixuan Ma, Heng Fan, Shuting He, Wenjia Liang, Daluo Mei, Xiaoyu Ma, Ran Li and 6 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Journal of neuroinflammation, 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

16 authors.

Hongtao Zhu *Department of Neurosurgery, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, No. 1095 Jiefang Avenue, Wuhan, 430030, China.
Lidong Cheng *Department of Neurosurgery, The Central Hospital of Wuhan, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.
Dan Liu *Department of Oncology, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.
Yixuan Ma *Department of Neurosurgery, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, No. 1095 Jiefang Avenue, Wuhan, 430030, China.
Heng FanDepartment of Neurosurgery, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, No. 1095 Jiefang Avenue, Wuhan, 430030, China.
Shuting HeDepartment of Neurosurgery, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, No. 1095 Jiefang Avenue, Wuhan, 430030, China.
Wenjia LiangDepartment of Neurosurgery, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, No. 1095 Jiefang Avenue, Wuhan, 430030, China.
Daluo MeiDepartment of Neurosurgery, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, No. 1095 Jiefang Avenue, Wuhan, 430030, China.
Xiaoyu MaDepartment of Neurosurgery, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, No. 1095 Jiefang Avenue, Wuhan, 430030, China.
Ran LiDepartment of Neurosurgery, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, No. 1095 Jiefang Avenue, Wuhan, 430030, China.
Hailong MiDepartment of Histology and Embryology, School of Basic Medicine, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.
Junwen WangDepartment of Neurosurgery, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, No. 1095 Jiefang Avenue, Wuhan, 430030, China.
Jun LiDepartment of Neurosurgery, The Central Hospital of Wuhan, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.
Xingjiang YuDepartment of Histology and Embryology, School of Basic Medicine, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China. yuxingjiang@hust.edu.cn.
Suojun ZhangDepartment of Neurosurgery, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, No. 1095 Jiefang Avenue, Wuhan, 430030, China. zhangsuojun@tjh.tjmu.edu.cn.
Kai ShuDepartment of Neurosurgery, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, No. 1095 Jiefang Avenue, Wuhan, 430030, China. kshu@tjh.tjmu.edu.cn.

Funding

Artificial Intelligence Program of Tongji Hospital AI2025B01China Postdoctoral Science Foundation 2022M711253China Postdoctoral Science Foundation 2024M761034Huazhong University of Science and Technology Independent Innovation Research Fund Project 2019kfyXJJS187Huazhong University of Science and Technology Young Scholars Program for Medical-Engineering Interdisciplinary Research 2025JCYJ053Hubei Association for Science and Technology Young Talents Support Projects 2024Hubei Natural Science Foundation 2023AFB135National Key R&D Program of China, MOST 2023YFC2510000National Natural Science Foundation of China 81974452National Natural Science Foundation of China 82072805National Natural Science Foundation of China 82403476National Natural Science Foundation of China 82503376
6 · The paper itself

Abstract

Tumor-associated macrophages (TAMs) symbiotically interact with glioma stem cells (GSCs) to facilitate GSCs stemness maintenance and glioblastoma (GBM) progression. Here we identified the complement 5a (C5a) as a key mediator of GSCs-TAMs symbiosis through integrative screening. C5a is preferentially expressed and secreted by GSCs. C5a activates the p-STAT3-cMyc-PD-L1 axis to promote GSCs proliferation, self-renewal and resistance against cytotoxic T cells through its receptor C5aR1. Moreover, GSCs-derived C5a trigger the infiltration and immunosuppressive polarization of TAMs through C5aR1-p-AKT T308 axis in tumor microenvironment. Importantly, silencing or pharmacological inhibition of C5a/C5aR1 disrupts both GSCs and TAMs and suppresses GBM tumor growth. In human GBM, the C5a/C5aR1 axis is activated and positively correlates with stemness, immunosuppressive TAMs and predicts poor prognosis. Collectively, these results demonstrate the key role of C5a/C5aR1 pathway in GSCs-TAMs symbiosis and indicate the therapeutic potential of targeting this pathway for GBM treatment.

Indexed as

Brain NeoplasmsComplement C5aGlioblastomaMacrophagesNeoplastic Stem CellsReceptor, Anaphylatoxin C5aSymbiosisTumor-Associated MacrophagesAnimalsCell Line, TumorDisease ProgressionHumansMiceSignal TransductionTumor MicroenvironmentC5AR1 protein, humanComplement C5aReceptor, Anaphylatoxin C5aComplement 5aGlioblastomaGlioma stem cellTumor-associated macrophageTumor-immune symbiosis

Identifiers

PMID42343442
PMCPMC13551683

What Socratic holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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 Socratic graph.