Evidence map›Paper›PMID 30301800›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2018

C-type lectin receptor LSECtin-mediated apoptotic cell clearance by macrophages directs intestinal repair in experimental colitis.

Zaopeng Yang, Qian Li, Xin Wang, Xuepei Jiang, Dianyuan Zhao, Xin Lin, Fuchu He, Li Tang

Open access · bronzeAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
1.8field-weighted citation impact, top 15% of its field
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

29 citing papers in PubMed, 45 citations in OpenAlex.

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  18. Can SARS-CoV-2 Virus Use Multiple Receptors to Enter Host Cells?International journal of molecular sciences · 2021
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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

8 authors at 4 institutions in 1 country.

Zaopeng YangState Key Laboratory of Proteomics, Beijing Proteome Research Center, National Center for Protein Sciences, Beijing Institute of Lifeomics, 102206 Beijing, China.
Qian LiInstitutes of Biomedical Sciences, Fudan University, 200032 Shanghai, China.
Xin WangState Key Laboratory of Proteomics, Beijing Proteome Research Center, National Center for Protein Sciences, Beijing Institute of Lifeomics, 102206 Beijing, China.
Xuepei JiangState Key Laboratory of Proteomics, Beijing Proteome Research Center, National Center for Protein Sciences, Beijing Institute of Lifeomics, 102206 Beijing, China.
Dianyuan ZhaoState Key Laboratory of Proteomics, Beijing Proteome Research Center, National Center for Protein Sciences, Beijing Institute of Lifeomics, 102206 Beijing, China.
Xin LinInstitute for Immunology, Tsinghua University-Peking University Joint Center for Life Sciences, Tsinghua University School of Medicine, 100084 Beijing, China.
Fuchu HeState Key Laboratory of Proteomics, Beijing Proteome Research Center, National Center for Protein Sciences, Beijing Institute of Lifeomics, 102206 Beijing, China; hefc@nic.bmi.ac.cn tangli08@aliyun.com.
Li TangState Key Laboratory of Proteomics, Beijing Proteome Research Center, National Center for Protein Sciences, Beijing Institute of Lifeomics, 102206 Beijing, China; hefc@nic.bmi.ac.cn tangli08@aliyun.com.
Beijing Proteome Research Center · CNFudan University · CNPeking University · CNTsinghua University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Epithelial barrier disruption is a major cause of inflammatory bowel disease (IBD); however, the cellular and molecular regulation of intestinal epithelial homeostasis remains largely undefined. Here, we show that the C-type lectin receptor LSECtin (Clec4g) on macrophages is required for protection against dextran sulfate sodium-induced colitis. Mechanistically, LSECtin promotes apoptotic cell clearance by macrophages and induces the production of antiinflammatory/tissue repair factors in an engulfment-dependent manner, which in turn stimulates epithelial cell proliferation. Deletion of LSECtin results in defective engulfment by colon macrophages, leading to aberrant proresolving factor production and impaired intestinal epithelium repair. Collectively, our findings suggest that LSECtin-dependent corpse clearance by macrophages can direct intestinal regeneration and maintenance of the mucosal barrier after injury.

Indexed as

AnimalsApoptosisCell ProliferationColitisColonDisease Models, AnimalEpithelial CellsInflammatory Bowel DiseasesIntestinal MucosaLectins, C-TypeMacrophagesMaleMiceMice, Inbred C57BLPhagocytosisReceptors, VirusLectins, C-TypeLSECtin protein, mouseReceptors, Virusapoptotic cell clearanceC-type lectin receptorintestinal regenerationmacrophage

Identifiers

PMID30301800
PMCPMC6205441
OpenAlexW2897988416

What OpenQuestion 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 OpenQuestion graph.