Evidence map›Paper›PMID 29251315›Full record

ArticleInternational journal of molecular medicine2018

Hepatic recruitment of CD11b+Ly6C+ inflammatory monocytes promotes hepatic ischemia/reperfusion injury.

Peng Song, Junbin Zhang, Yunwei Zhang, Zhiping Shu, Peng Xu, Long He, Chao Yang, Jinxiang Zhang, Hui Wang, Yiqing Li and 1 more

Abstract read
In one paragraph

Article in International journal of molecular medicine, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing 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

23 citing papers in PubMed.

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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

11 authors.

Peng SongDepartment of Vascular Surgery, Union Hospital, Huazhong University of Science and Technology, Wuhan, Hubei 430033 P.R. China.
Junbin ZhangDepartment of Emergency Surgery, Union Hospital, Huazhong University of Science and Technology, Wuhan, Hubei 430033 P.R. China.
Yunwei ZhangDepartment of Emergency Surgery, Union Hospital, Huazhong University of Science and Technology, Wuhan, Hubei 430033 P.R. China.
Zhiping ShuDepartment of Nuclear Medicine, Tongji Hospital, Huazhong University of Science and Technology, Wuhan, Hubei 430033 P.R. China.
Peng XuDepartment of Emergency Surgery, Union Hospital, Huazhong University of Science and Technology, Wuhan, Hubei 430033 P.R. China.
Long HeDepartment of Clinical Laboratory, Puai Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei 430033 P.R. China.
Chao YangDepartment of Vascular Surgery, Union Hospital, Huazhong University of Science and Technology, Wuhan, Hubei 430033 P.R. China.
Jinxiang ZhangDepartment of Emergency Surgery, Union Hospital, Huazhong University of Science and Technology, Wuhan, Hubei 430033 P.R. China.
Hui WangDepartment of Genetics, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei 430033 P.R. China.
Yiqing LiDepartment of Vascular Surgery, Union Hospital, Huazhong University of Science and Technology, Wuhan, Hubei 430033 P.R. China.
Qin LiDepartment of Vascular Surgery, Union Hospital, Huazhong University of Science and Technology, Wuhan, Hubei 430033 P.R. China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Monocytes infiltrate damaged liver tissue during noninfectious liver injury and often have dual roles, perpetuating inflammation and promoting resolution of inflammation and fibrosis. However, how monocyte subsets distribute and are differentially recruited in the liver remain unclear. In the current study, the subpopulations of infiltrating monocytes were examined following liver ischemia/reperfusion (I/R) injury in mice using flow cytometry. CD11b+Ly6C high (Ly6Chi) cells (inflammatory monocytes) and CD11b+Ly6C low cells (reparative monocytes) were recruited into the liver following I/R injury. Treatment with clodronate‑loaded liposomes, which transiently deplete systemic macrophages, alleviated hepatic damage. Mice genetically deficient in C‑C motif chemokine ligand 2 (CCL2), or its receptor C‑C chemokine receptor 2 (CCR2), exhibited diminished hepatic damage compared with wild‑type mice following I/R, by controlling intrahepatic inflammatory Ly6Chi monocyte accumulation. In addition, the CCR2 specific inhibitor RS504393 alleviated hepatic I/R injury. The results suggest that the CCR2/CCL2 axis has an important role in monocyte infiltration and may represent a novel target for the treatment of liver I/R injury.

Indexed as

AnimalsAntigens, LyCD11b AntigenChemokine CCL2Clodronic AcidFlow CytometryInflammationLiverMaleMiceMice, Inbred C57BLMonocytesReceptors, CCR2Reperfusion InjuryReverse Transcriptase Polymerase Chain ReactionAntigens, LyCcr2 protein, mouseCD11b AntigenChemokine CCL2Clodronic AcidLy-6C antigen, mouseReceptors, CCR2

Identifiers

PMID29251315
PMCPMC5752159

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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.