Evidence map›Paper›PMID 35069982›Full record

ArticleOxidative medicine and cellular longevity2022

Advanced Glycation End Products Induce Atherosclerosis via RAGE/TLR4 Signaling Mediated-M1 Macrophage Polarization-Dependent Vascular Smooth Muscle Cell Phenotypic Conversion.

Yujie Xing, Shuo Pan, Ling Zhu, Qianwei Cui, Zhiguo Tang, Zhongwei Liu, Fuqiang Liu

Open access · hybridAbstract read
In one paragraph

Article in Oxidative medicine and cellular longevity, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed
7.0field-weighted citation impact, top 2% 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

34 citing papers in PubMed, 56 citations in OpenAlex.

  1. Review
  2. Hepatocyte BDNF Acts as a Novel Immune Checkpoint to Restrain TLR4-Mediated Acute Hepatitis.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026
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  7. RAGE deficiency ameliorates abdominal aortic aneurysm progression.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2025
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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

7 authors at 2 institutions in 1 country.

Yujie XingDepartment of Cardiology, Shaanxi Provincial People's Hospital, Xi'an, China.ORCID https://orcid.org/0000-0002-0075-9338
Shuo PanDepartment of Cardiology, Shaanxi Provincial People's Hospital, Xi'an, China.ORCID https://orcid.org/0000-0002-0271-5072
Ling ZhuDepartment of Cardiology, Shaanxi Provincial People's Hospital, Xi'an, China.ORCID https://orcid.org/0000-0002-6559-0967
Qianwei CuiDepartment of Cardiology, Shaanxi Provincial People's Hospital, Xi'an, China.
Zhiguo TangDepartment of Cardiology, Shaanxi Provincial People's Hospital, Xi'an, China.ORCID https://orcid.org/0000-0002-0360-6396
Zhongwei LiuDepartment of Cardiology, Shaanxi Provincial People's Hospital, Xi'an, China.ORCID https://orcid.org/0000-0002-5548-5450
Fuqiang LiuDepartment of Cardiology, Shaanxi Provincial People's Hospital, Xi'an, China.ORCID https://orcid.org/0000-0003-0371-639X
Shanxi Medical University · CNNorthwestern Polytechnical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectiveThe objective of this study was to investigate the involved mechanisms of advanced glycation end product- (AGE-) exacerbated atherosclerosis (AS).

methodsToll-like receptor 4 (TLR4) inhibitor was administrated to type 2 diabetes mellitus (T2DM) AS rats. Atherosclerotic plaque, M1 macrophage infiltration, and VSMCs phenotypes were evaluated. AGE-exposed primary macrophages were treated with specific siRNAs knocking down receptor for AGEs (RAGE) and TLR4. Phenotypes of M1 macrophage and VSMCs were identified by fluorescent stains. Contact and noncontact coculture models were established. VSMCs and macrophages were cocultured in these models. ELISA was used to detect inflammatory cytokine concentrations. Relative mRNA expression levels were determined by real-time PCR. Relative protein expression and phosphorylation levels were evaluated by Western blots assays.

resultsTLR4 inhibitor treatment significantly reduced arterial stenosis, infiltration of M1 polarized macrophages, and contractile-to-synthetic phenotype conversion of VSMCs in DM AS animals.

conclusionsAGEs induced activation of RAGE/TLR4/FOXC2 signaling, which featured macrophage with Dll4 high expression during M1 polarization. These macrophages promoted contractile-synthetic phenotypic conversion of VSMCs through the Dll4/Notch pathway after direct cell-to-cell contacts.

Indexed as

AnimalsAtherosclerosisGlycation End Products, AdvancedHumansMacrophagesMaleMicePhenotypeSignal TransductionToll-Like Receptor 4TransfectionGlycation End Products, AdvancedTlr4 protein, mouseToll-Like Receptor 4

Identifiers

PMID35069982
PMCPMC8776434
OpenAlexW4206657724

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Registered trials

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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.