Evidence map›Paper›PMID 41266856›Full record

ArticleCell biology and toxicology2025

SENP3 mediated DeSUMOylation of macrophage derived CCL17 accelerates atherosclerosis via regulation of Treg.

Xiliang Zhao, Fenfang Zhang, Jianjun Du, Yaodong Ding, Yang Zhang, Yong Zeng, Yicong Ye

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Cell biology and toxicology, 2025. 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

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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

7 authors.

Xiliang ZhaoDepartment of Cardiology, Beijing Anzhen Hospital, Capital Medical University, No.2, Anzhen Road Chaoyang District, Beijing, 100029, People's Republic of China.
Fenfang ZhangDepartment of Cardiology, Yangquan First People's Hospital, Yangquan, 045000, People's Republic of China.
Jianjun DuDepartment of Cardiology, The First People's Hospital of Keerqin District, Tongliao, 028000, People's Republic of China.
Yaodong DingDepartment of Cardiology, Beijing Anzhen Hospital, Capital Medical University, No.2, Anzhen Road Chaoyang District, Beijing, 100029, People's Republic of China.
Yang ZhangDepartment of Cardiology, Beijing Anzhen Hospital, Capital Medical University, No.2, Anzhen Road Chaoyang District, Beijing, 100029, People's Republic of China.
Yong ZengDepartment of Cardiology, Beijing Anzhen Hospital, Capital Medical University, No.2, Anzhen Road Chaoyang District, Beijing, 100029, People's Republic of China.
Yicong YeDepartment of Cardiology, Beijing Anzhen Hospital, Capital Medical University, No.2, Anzhen Road Chaoyang District, Beijing, 100029, People's Republic of China. yicongye@163.com.

Funding

Beijing Hospital Authority Incubating Program PX2021028National Natural Science Foundation of China 82200370
6 · The paper itself

Abstract

backgroundAtherosclerosis (AS) is a cardiovascular problem, which is featured by the accumulation of lipids in the intimal layer of the arterial wall and inflammatory reaction of immune cells. CCL17 is an inflammatory mediator associated with promoting AS. Nevertheless, the specific role of CCL17 and its upstream regulatory mechanisms in macrophage mediated inflammation and AS remain unclear.

methodsAn AS mice model was established by subjecting ApoE

resultsThe CCL17 and SENP3 expression in plaque sample of AS mice were significantly up-regulated. Knocking down CCL17 or SENP3 in mice could reverse the vascular damage, lipid accumulation, the increase of the blood lipid levels and the increase of inflammatory reaction in AS mice. On the molecular mechanism level, SENP3 increased the protein stability of CCL17 and thus increased CCL17 expression by DeSUMOylation modification at K115 site of CCL17 protein. In macrophages induced by oxLDL, CCL17 and CCL22 affect the chemotaxis of Treg competitively.

conclusionThis study showed that SENP3 mediated deSUMOylation of CCL17, increase CCL17 expression in macrophage. CCL17 secreted by macrophage regulating Treg recruitment through the competitive interaction between CCL17 and CCL22 and thus aggravated AS. Our findings provide a new regulatory mechanism and potential target for AS treatment.

Indexed as

AtherosclerosisChemokine CCL17Cysteine EndopeptidasesMacrophagesT-Lymphocytes, RegulatoryAnimalsDiet, High-FatDisease Models, AnimalLipoproteins, LDLMaleMiceMice, Inbred C57BLCcl17 protein, mouseChemokine CCL17Cysteine EndopeptidasesLipoproteins, LDLoxidized low density lipoproteinSenp3 protein, mouseAtherosclerosisCCL17InflammationLipid accumulationMacrophages

Identifiers

PMID41266856
PMCPMC12634754

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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.