Evidence map›Paper›PMID 41350870›Full record

ArticleJournal of neuroinflammation2025

Soluble CSF1R alleviates microgliopathy in a CSF1R-related leukoencephalopathy (CRL) mouse model.

Yuhang Zhou, Banglian Hu, Jie Luo, Xingyi Wang, Xiaohua Huang, Yanfang Li, Xian Zhang, Guojun Bu, Hongsheng Zhang, Yun-Wu Zhang and 1 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Journal of neuroinflammation, 2025. 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

11 authors.

Yuhang ZhouXiamen Key Laboratory of Brain Center, The First Affiliated Hospital of Xiamen University, Fujian Provincial Key Laboratory of Neurodegenerative Disease and Aging Research, Institute of Neuroscience, School of Medicine, Xiamen University, Xiamen, Fujian, 361102, China.
Banglian HuXiamen Key Laboratory of Brain Center, The First Affiliated Hospital of Xiamen University, Fujian Provincial Key Laboratory of Neurodegenerative Disease and Aging Research, Institute of Neuroscience, School of Medicine, Xiamen University, Xiamen, Fujian, 361102, China.
Jie LuoXiamen Key Laboratory of Brain Center, The First Affiliated Hospital of Xiamen University, Fujian Provincial Key Laboratory of Neurodegenerative Disease and Aging Research, Institute of Neuroscience, School of Medicine, Xiamen University, Xiamen, Fujian, 361102, China.
Xingyi WangXiamen Key Laboratory of Brain Center, The First Affiliated Hospital of Xiamen University, Fujian Provincial Key Laboratory of Neurodegenerative Disease and Aging Research, Institute of Neuroscience, School of Medicine, Xiamen University, Xiamen, Fujian, 361102, China.
Xiaohua HuangBasic Medical Sciences, School of Medicine, Xiamen University, Xiamen, Fujian, 361102, China.
Yanfang LiXiamen Key Laboratory of Brain Center, The First Affiliated Hospital of Xiamen University, Fujian Provincial Key Laboratory of Neurodegenerative Disease and Aging Research, Institute of Neuroscience, School of Medicine, Xiamen University, Xiamen, Fujian, 361102, China.
Xian ZhangXiamen Key Laboratory of Brain Center, The First Affiliated Hospital of Xiamen University, Fujian Provincial Key Laboratory of Neurodegenerative Disease and Aging Research, Institute of Neuroscience, School of Medicine, Xiamen University, Xiamen, Fujian, 361102, China.
Guojun BuDivision of Life Science and State Key Laboratory of Nervous System Disorders, The Hong Kong University of Science and Technology, Clear Water Bay, Hong Kong, China.
Hongsheng ZhangXiamen Key Laboratory of Brain Center, The First Affiliated Hospital of Xiamen University, Fujian Provincial Key Laboratory of Neurodegenerative Disease and Aging Research, Institute of Neuroscience, School of Medicine, Xiamen University, Xiamen, Fujian, 361102, China. hszhang@cqmu.edu.cn.
Yun-Wu ZhangXiamen Key Laboratory of Brain Center, The First Affiliated Hospital of Xiamen University, Fujian Provincial Key Laboratory of Neurodegenerative Disease and Aging Research, Institute of Neuroscience, School of Medicine, Xiamen University, Xiamen, Fujian, 361102, China. yunzhang@xmu.edu.cn.
Honghua ZhengXiamen Key Laboratory of Brain Center, The First Affiliated Hospital of Xiamen University, Fujian Provincial Key Laboratory of Neurodegenerative Disease and Aging Research, Institute of Neuroscience, School of Medicine, Xiamen University, Xiamen, Fujian, 361102, China. honghua@xmu.edu.cn.

Funding

CQMU Program for Youth Innovation in Future Medicine W0158National Natural Science Foundation of China 82271219National Natural Science Foundation of China 82271472Natural Science Foundation of Fujian Province 2021J01016Natural Science Foundation Project of Chongqing, Chongqing Science and Technology Commission CSTB2022NSCQ-LZX0033the program of Lin Gang Laboratory LGL-ADB120102
6 · The paper itself

Abstract

Colony-stimulating factor 1 receptor (CSF1R), primarily expressed on microglia in the central nervous system (CNS), is essential for microglial homeostasis and survival. CSF1R dysfunction, due to a monoallelic mutation, causes CSF1R-related leukoencephalopathy (CRL), a primary microgliopathy. CSF1R undergoes proteolytic cleavage to release soluble CSF1R (sCSF1R), which is decreased in the serum of CRL patients. However, the biological function of sCSF1R remains unknown. Here, we found that sCSF1R alleviated cognitive impairment and anxiety-like behavior in Csf1r+/− mice. Importantly, we identified CSF1R as a target binding protein of sCSF1R on microglia. Notably, sCSF1R inhibited the activation and inflammatory factor expression of Csf1r+/− microglia by reducing the phosphorylation of CSF1R (Y723) and NF-κB (S468 and S536). These results demonstrate that sCSF1R exerts neuroprotective effects by binding membrane-bound CSF1R and inhibiting pathological microglial activation by inhibiting the nuclear translocation of NF-κB. These findings identify sCSF1R as a potential therapeutic agent for CRL.

Indexed as

LeukoencephalopathiesMicrogliaReceptors, Granulocyte-Macrophage Colony-Stimulating FactorAnimalsDisease Models, AnimalHumansMaleMiceMice, Inbred C57BLMice, KnockoutCsf1r protein, mouseReceptors, Granulocyte-Macrophage Colony-Stimulating FactorCRLCSF1RMicrogliopathySoluble CSF1R

Identifiers

PMID41350870
PMCPMC12797715

What Socratic holds

Textmetadata
LicenceCC BY
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.