Evidence map›Paper›PMID 40490565›Full record

ArticleCellular and molecular life sciences : CMLS2025

CMTM7 inhibits TLR4 signaling pathway via promoting Rab5 activation and alleviates acute liver injury.

Yingzhe Sun, Zixia Guo, Yangbo Huo, Hanxiao Zhang, Ting Li, Pingzhang Wang, Wenling Han

Abstract read
In one paragraph

Article in Cellular and molecular life sciences : CMLS, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing 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

2 citing papers in PubMed.

  1. Article
  2. Article
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

7 authors.

Yingzhe SunDepartment of Immunology, School of Basic Medical Sciences, NHC Key Laboratory of Medical Immunology, Peking University Health Science Center, Beijing, China.
Zixia GuoDepartment of Immunology, School of Basic Medical Sciences, NHC Key Laboratory of Medical Immunology, Peking University Health Science Center, Beijing, China.
Yangbo HuoDepartment of Immunology, School of Basic Medical Sciences, NHC Key Laboratory of Medical Immunology, Peking University Health Science Center, Beijing, China.
Hanxiao ZhangDepartment of Immunology, School of Basic Medical Sciences, NHC Key Laboratory of Medical Immunology, Peking University Health Science Center, Beijing, China.
Ting LiDepartment of Immunology, School of Basic Medical Sciences, NHC Key Laboratory of Medical Immunology, Peking University Health Science Center, Beijing, China.
Pingzhang WangDepartment of Immunology, School of Basic Medical Sciences, NHC Key Laboratory of Medical Immunology, Peking University Health Science Center, Beijing, China.
Wenling HanDepartment of Immunology, School of Basic Medical Sciences, NHC Key Laboratory of Medical Immunology, Peking University Health Science Center, Beijing, China. hanwl@bjmu.edu.cn.ORCID http://orcid.org/0000-0002-9548-4524

Funding

China General Technology Research Institute GZKJ-KJXX-QTHT-20230626National Natural Science Foundation of China 81971472National Natural Science Foundation of China 82171750
6 · The paper itself

Abstract

The activation of macrophages mediated by TLR4 is crucial for innate immune responses, while the regulatory mechanisms of TLR4 are still under investigation. This study demonstrates that CMTM7 inhibits TLR4 pathway activation in macrophages and exerts a protective role in acute liver injury (ALI). CMTM7 is highly expressed in monocytes/macrophages, which is downregulated upon LPS stimulation. CMTM7 inhibits LPS/HMGB1-induced activation of the TLR4 pathway in macrophages. Mechanistically, CMTM7 promotes the binding between Rab5 and Gapex5, leading to the generation of GTP-Rab5, which facilitates the internalization and degradation of TLR4, thereby inhibiting TLR4 signaling activation. Utilizing Cmtm7 myeloid conditional knockout mice, we confirmed the protective role of CMTM7 in ALI and highlighted its therapeutic potential through the adoptive transfer of CMTM7-overexpressing macrophages. This study elucidates a novel regulatory mechanism of TLR4 signaling transduction and provides a novel therapeutic strategy for ALI treatment.

Indexed as

MARVEL Domain-Containing ProteinsMyelin Proteinsrab5 GTP-Binding ProteinsSignal TransductionToll-Like Receptor 4AnimalsHumansLipopolysaccharidesMacrophagesMaleMiceMice, Inbred C57BLMice, KnockoutRAW 264.7 CellsLipopolysaccharidesMARVEL Domain-Containing ProteinsMyelin Proteinsrab5 GTP-Binding ProteinsTlr4 protein, mouseToll-Like Receptor 4ALICMTM7Gapex5MacrophageRab5TLR4

Identifiers

PMID40490565
PMCPMC12149389

What OpenQuestion holds

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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.