Evidence map›Paper›PMID 35842658›Full record

ArticleJournal of translational medicine2022

A reduction of Syndecan-4 in macrophages promotes atherosclerosis by aggravating the proinflammatory capacity of macrophages.

Jiaxin Hu, Ying Zhang, Liaoping Hu, Haiting Chen, Han Wu, Jianzhou Chen, Jun Xie, Biao Xu, Zhonghai Wei

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Journal of translational medicine, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
0.8field-weighted citation impact, top 32% 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

5 citing papers in PubMed, 11 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

9 authors at 1 institution in 1 country.

Jiaxin Hu *Department of Cardiology, MOE Key Laboratory of Model Animal for Disease Study, Nanjing Drum Tower Hospital, The Affiliated Hospital of Nanjing University Medical School, Nanjing University, Nanjing, 210061, China.
Ying Zhang *Department of Cardiology, MOE Key Laboratory of Model Animal for Disease Study, Nanjing Drum Tower Hospital, The Affiliated Hospital of Nanjing University Medical School, Nanjing University, Nanjing, 210061, China.
Liaoping Hu *Department of Cardiology, MOE Key Laboratory of Model Animal for Disease Study, Nanjing Drum Tower Hospital, The Affiliated Hospital of Nanjing University Medical School, Nanjing University, Nanjing, 210061, China.
Haiting Chen *Department of Cardiology, MOE Key Laboratory of Model Animal for Disease Study, Nanjing Drum Tower Hospital, The Affiliated Hospital of Nanjing University Medical School, Nanjing University, Nanjing, 210061, China.
Han WuDepartment of Cardiology, MOE Key Laboratory of Model Animal for Disease Study, Nanjing Drum Tower Hospital, The Affiliated Hospital of Nanjing University Medical School, Nanjing University, Nanjing, 210061, China.
Jianzhou ChenDepartment of Cardiology, MOE Key Laboratory of Model Animal for Disease Study, Nanjing Drum Tower Hospital, The Affiliated Hospital of Nanjing University Medical School, Nanjing University, Nanjing, 210061, China.
Jun XieDepartment of Cardiology, MOE Key Laboratory of Model Animal for Disease Study, Nanjing Drum Tower Hospital, The Affiliated Hospital of Nanjing University Medical School, Nanjing University, Nanjing, 210061, China.
Biao XuDepartment of Cardiology, MOE Key Laboratory of Model Animal for Disease Study, Nanjing Drum Tower Hospital, The Affiliated Hospital of Nanjing University Medical School, Nanjing University, Nanjing, 210061, China. xubiao62@nju.edu.cn.
Zhonghai WeiDepartment of Cardiology, MOE Key Laboratory of Model Animal for Disease Study, Nanjing Drum Tower Hospital, The Affiliated Hospital of Nanjing University Medical School, Nanjing University, Nanjing, 210061, China. weizhonghai@njglyy.com.
Nanjing Drum Tower Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundCardiovascular diseases (CVDs) are a significant cause of mortality worldwide and are characterized by severe atherosclerosis (AS) in patients. However, the molecular mechanism of AS formation remains elusive. In the present study, we investigated the role of syndecan-4 (SDC4), a member of the syndecan family, in atherogenesis. METHODS AND

resultsThe expression of SDC4 decreased in mouse severe AS models. Moreover, knockout of SDC4 accelerated high-cholesterol diets (HCD)-induced AS in ApoE

conclusionThese findings provide evidence that SDC4 reduction links macrophages and inflammation to AS and that SDC4 in macrophages provides a therapeutic target for preventing AS formation.

Indexed as

AtherosclerosisAnimalsApolipoproteins ECholesterolDisease Models, AnimalMacrophagesMiceMice, KnockoutSyndecan-4Apolipoproteins ECholesterolSdc4 protein, mouseSyndecan-4ApoE−/−AtherosclerosisMacrophageOx-LDLSyndecan-4

Identifiers

PMID35842658
PMCPMC9287986
OpenAlexW4285587274

What OpenQuestion holds

Textmetadata
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.