Evidence map›Paper›PMID 41792769›Full record

ArticleJournal of neuroinflammation2026

APOE-mediated lipid transport prevents C1q-related synaptic loss after spinal cord injury via attenuating macrophage lipid stress.

Yersen Mulat, Zun Ren, Chaocao Nong, Chuanliang Fu, Yilin Huo, Mai Zhao, Yahui Dai, Canyu Chen, Peilin Wang, Renyuan Wang and 7 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

17 authors.

Yersen Mulat *Trauma Center, Shanghai General Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, 201620, China.
Zun Ren *Trauma Center, Shanghai General Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, 201620, China.
Chaocao Nong *Trauma Center, Shanghai General Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, 201620, China.
Chuanliang FuTrauma Center, Shanghai General Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, 201620, China.
Yilin HuoTrauma Center, Shanghai General Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, 201620, China.
Mai ZhaoTrauma Center, Shanghai General Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, 201620, China.
Yahui DaiTrauma Center, Shanghai General Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, 201620, China.
Canyu ChenTrauma Center, Shanghai General Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, 201620, China.
Peilin WangTrauma Center, Shanghai General Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, 201620, China.
Renyuan WangTrauma Center, Shanghai General Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, 201620, China.
Hao ZhangTrauma Center, Shanghai General Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, 201620, China.
Yi HuTrauma Center, Shanghai General Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, 201620, China.
Peng LaiTrauma Center, Shanghai General Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, 201620, China.
Ruoyi GuoTrauma Center, Shanghai General Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, 201620, China.
Dongsheng JiangTrauma Center, Shanghai General Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, 201620, China. dongsheng.jiang@sjtu.edu.cn.
Ying PengTrauma Center, Shanghai General Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, 201620, China. 13122177028@163.com.
Haodong LinTrauma Center, Shanghai General Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, 201620, China. 72400019193@shsmu.edu.cn.

Funding

Excellent Academic Leader Project of Shanghai Science and Technology Commission 22XD1402600National Natural Science Foundation of China NSFC 82271407National Natural Science Foundation of China NSFC 82501639
6 · The paper itself

Abstract

Following spinal cord injury (SCI), neuroinflammation driven by lipid-laden macrophage foam cells is a key pathology, yet how these cells manage their lipid homeostasis is unclear. We delineate a neuroprotective axis in which macrophages deploy apolipoprotein E (APOE) to transfer intracellular lipids to neighboring cells, especially fibroblasts. Genetic ablation of Apoe disrupts this intercellular lipid transport, culminating in pathological lipid retention that activates the Hippo signalling cascade and transcriptionally induces complement component C1q. This excess C1q aberrantly tags intact synapses for excessive microglial pruning, leading to significant synaptic loss and impaired locomotor function recovery. Direct blockade of C1q using neutralizing antibodies recapitulated these neuroprotective effects, confirming C1q as the critical mediator. Crucially, macrophage-specific APOE re-expression reverses this entire cascade, preserving synapses and restoring locomotor function (BMS score: 4.81 ± 0.21 (Apoe) vs. 1.75 ± 1.28 (NC); Incline plane: 69.24° ± 2.33° (Apoe) vs. 51.66° ± 5.14° (NC) in Apoe−/− mice). These findings identify the APOE-Hippo-C1q pathway in macrophages as a novel therapeutic target for SCI.

Indexed as

Apolipoproteins EComplement C1qLipid MetabolismMacrophagesSpinal Cord InjuriesSynapsesAnimalsBiological TransportMiceMice, Inbred C57BLMice, KnockoutApolipoproteins EComplement C1q

Identifiers

PMID41792769
PMCPMC13077989

What OpenQuestion holds

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LicenceCC BY-NC-ND
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 OpenQuestion graph.