Evidence map›Paper›PMID 34189838›Full record

ArticleJournal of cellular and molecular medicine2021

CCL7 contributes to angiotensin II-induced abdominal aortic aneurysm by promoting macrophage infiltration and pro-inflammatory phenotype.

Cuiping Xie, Feiming Ye, Ning Zhang, Yuxue Huang, Yun Pan, Xiaojie Xie

Open access · goldAbstract read
In one paragraph

Article in Journal of cellular and molecular medicine, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed
4.4field-weighted citation impact, top 5% 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

32 citing papers in PubMed, 45 citations in OpenAlex.

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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

6 authors at 2 institutions in 1 country.

Cuiping XieDepartment of Cardiology, Cardiovascular Key Laboratory of Zhejiang Province, Zhejiang University School of Medicine Second Affiliated Hospital, Hangzhou, China.
Feiming YeDepartment of Cardiology, Cardiovascular Key Laboratory of Zhejiang Province, Zhejiang University School of Medicine Second Affiliated Hospital, Hangzhou, China.
Ning ZhangDepartment of Cardiology, Cardiovascular Key Laboratory of Zhejiang Province, Zhejiang University School of Medicine Second Affiliated Hospital, Hangzhou, China.
Yuxue HuangDepartment of Cardiology, Cardiovascular Key Laboratory of Zhejiang Province, Zhejiang University School of Medicine Second Affiliated Hospital, Hangzhou, China.
Yun PanCollege of Information Science and Electronic Engineering, Zhejiang University, Hangzhou, China.
Xiaojie XieDepartment of Cardiology, Cardiovascular Key Laboratory of Zhejiang Province, Zhejiang University School of Medicine Second Affiliated Hospital, Hangzhou, China.ORCID 0000-0001-8421-2737
Second Affiliated Hospital of Zhejiang University · CNZhejiang University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Chemokine C-C motif ligand 7 (CCL7), a member of CC chemokine subfamily, plays pivotal roles in numerous inflammatory diseases. Hyper-activation of inflammation is an important characteristic of abdominal aortic aneurysm (AAA). Therefore, in the present study, we aimed to determine the effect of CCL7 on AAA formation. CCL7 abundance in aortic tissue and macrophage infiltration were both increased in angiotensin II (Ang II)-induced AAA mice. Ex vivo, CCL7 promoted macrophage polarization towards M1 phenotype. This effect was reversed by the blockage of CCR1, a receptor of CCL7. CCL7 up-regulated JAK2/STAT1 protein level in macrophage, and CCL7-induced M1 activation was suppressed by JAK2/STAT1 pathway inhibition. To verify the effect of CCL7 on AAA in vivo, either CCL7-neutralizing antibody (CCL7-nAb) or vehicles were intraperitoneally injected 24 hours prior to Ang II infusion and subsequently every three days for 4 weeks. CCL7-nAb administration significantly attenuated Ang II-induced luminal and external dilation as well as pathological remodelling. Immunostaining showed that CCL7-nAb administration significantly decreased aneurysmal macrophage infiltration. In conclusion, CCL7 contributed to Ang II-induced AAA by promoting M1 phenotype of macrophage through CCR1/JAK2/STAT1 signalling pathway.

Indexed as

Cell MovementAngiotensin IIAnimalsAortic Aneurysm, AbdominalCell DifferentiationCells, CulturedChemokine CCL7HumansHuman Umbilical Vein Endothelial CellsJanus Kinase 2MacrophagesMaleMiceMice, Inbred C57BLPhenotypeReceptors, CCR1Angiotensin IICcl7 protein, mouseCcr1 protein, mouseChemokine CCL7Jak2 protein, mouseJanus Kinase 2Receptors, CCR1Stat1 protein, mouseSTAT1 Transcription Factorabdominal aortic aneurysmangiotensin IIChemokine C-C motif ligand 7M1 phenotypemacrophage

Identifiers

PMID34189838
PMCPMC8335673
OpenAlexW3177197876

What OpenQuestion holds

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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 OpenQuestion graph.