Evidence map›Paper›PMID 36585108›Full record

ArticleJournal of advanced research2023

SOX4 is a novel phenotypic regulator of endothelial cells in atherosclerosis revealed by single-cell analysis.

Chak Kwong Cheng, Xiao Lin, Yujie Pu, Joyce Ka Yu Tse, Yu Wang, Cheng-Lin Zhang, Xiaoyun Cao, Chi Wai Lau, Juan Huang, Lei He and 10 more

Open access · goldAbstract read
In one paragraph

Article in Journal of advanced research, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.

0numbers the graph read from it
0cells of the map it votes in
39citing papers in PubMed
3.7field-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

39 citing papers in PubMed, 51 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

20 authors at 5 institutions in 3 countries.

Chak Kwong ChengSchool of Biomedical Sciences and Li Ka Shing Institute of Health Science, The Chinese University of Hong Kong, 999077, Hong Kong Special Administrative Region; Heart and Vascular Institute and Shenzhen Research Institute, The Chinese University of Hong Kong, 999077, Hong Kong Special Administrative Region; Department of Biomedical Sciences, City University of Hong Kong, 999077, Hong Kong Special Administrative Region.
Xiao LinSchool of Life Sciences, The Chinese University of Hong Kong, 999077, Hong Kong Special Administrative Region.
Yujie PuSchool of Biomedical Sciences and Li Ka Shing Institute of Health Science, The Chinese University of Hong Kong, 999077, Hong Kong Special Administrative Region; Heart and Vascular Institute and Shenzhen Research Institute, The Chinese University of Hong Kong, 999077, Hong Kong Special Administrative Region.
Joyce Ka Yu TseSchool of Life Sciences, The Chinese University of Hong Kong, 999077, Hong Kong Special Administrative Region.
Yu WangSchool of Biomedical Sciences and Li Ka Shing Institute of Health Science, The Chinese University of Hong Kong, 999077, Hong Kong Special Administrative Region; Heart and Vascular Institute and Shenzhen Research Institute, The Chinese University of Hong Kong, 999077, Hong Kong Special Administrative Region.
Cheng-Lin ZhangSchool of Biomedical Sciences and Li Ka Shing Institute of Health Science, The Chinese University of Hong Kong, 999077, Hong Kong Special Administrative Region; Heart and Vascular Institute and Shenzhen Research Institute, The Chinese University of Hong Kong, 999077, Hong Kong Special Administrative Region.
Xiaoyun CaoSchool of Biomedical Sciences and Li Ka Shing Institute of Health Science, The Chinese University of Hong Kong, 999077, Hong Kong Special Administrative Region; Heart and Vascular Institute and Shenzhen Research Institute, The Chinese University of Hong Kong, 999077, Hong Kong Special Administrative Region.
Chi Wai LauSchool of Biomedical Sciences and Li Ka Shing Institute of Health Science, The Chinese University of Hong Kong, 999077, Hong Kong Special Administrative Region; Heart and Vascular Institute and Shenzhen Research Institute, The Chinese University of Hong Kong, 999077, Hong Kong Special Administrative Region.
Juan HuangSchool of Biomedical Sciences and Li Ka Shing Institute of Health Science, The Chinese University of Hong Kong, 999077, Hong Kong Special Administrative Region; Heart and Vascular Institute and Shenzhen Research Institute, The Chinese University of Hong Kong, 999077, Hong Kong Special Administrative Region.
Lei HeSchool of Biomedical Sciences and Li Ka Shing Institute of Health Science, The Chinese University of Hong Kong, 999077, Hong Kong Special Administrative Region; Heart and Vascular Institute and Shenzhen Research Institute, The Chinese University of Hong Kong, 999077, Hong Kong Special Administrative Region.
Jiang-Yun LuoSchool of Biomedical Sciences and Li Ka Shing Institute of Health Science, The Chinese University of Hong Kong, 999077, Hong Kong Special Administrative Region; Heart and Vascular Institute and Shenzhen Research Institute, The Chinese University of Hong Kong, 999077, Hong Kong Special Administrative Region.
Yu-Tsung ShihInstitute of Cellular and System Medicine, National Health Research Institutes, Miaoli 35053, Taiwan.
Song WanDepartment of Surgery, The Chinese University of Hong Kong, 999077, Hong Kong Special Administrative Region.
Chi Fai NgDepartment of Surgery, The Chinese University of Hong Kong, 999077, Hong Kong Special Administrative Region.
Li WangSchool of Biomedical Sciences and Li Ka Shing Institute of Health Science, The Chinese University of Hong Kong, 999077, Hong Kong Special Administrative Region; Heart and Vascular Institute and Shenzhen Research Institute, The Chinese University of Hong Kong, 999077, Hong Kong Special Administrative Region.
Ronald Ching Wan MaDepartment of Medicine and Therapeutics, The Chinese University of Hong Kong, 999077, Hong Kong Special Administrative Region; Hong Kong Institute of Diabetes and Obesity, The Chinese University of Hong Kong, 999077, Hong Kong Special Administrative Region.
Jeng-Jiann ChiuInstitute of Cellular and System Medicine, National Health Research Institutes, Miaoli 35053, Taiwan; School of Medical Laboratory Science and Biotechnology, College of Medical Science and Technology, Taipei Medical University, Taipei 11031, Taiwan.
Ting Fung ChanSchool of Life Sciences, The Chinese University of Hong Kong, 999077, Hong Kong Special Administrative Region.
Xiao Yu TianSchool of Biomedical Sciences and Li Ka Shing Institute of Health Science, The Chinese University of Hong Kong, 999077, Hong Kong Special Administrative Region; Heart and Vascular Institute and Shenzhen Research Institute, The Chinese University of Hong Kong, 999077, Hong Kong Special Administrative Region. Electronic address: xytian@cuhk.edu.hk.
Yu HuangSchool of Biomedical Sciences and Li Ka Shing Institute of Health Science, The Chinese University of Hong Kong, 999077, Hong Kong Special Administrative Region; Heart and Vascular Institute and Shenzhen Research Institute, The Chinese University of Hong Kong, 999077, Hong Kong Special Administrative Region; Department of Biomedical Sciences, City University of Hong Kong, 999077, Hong Kong Special Administrative Region. Electronic address: yu.huang@cityu.edu.hk.
Chinese University of Hong Kong, Shenzhen · CNChinese University of Hong Kong · CNCity University of Hong Kong · HKNational Health Research Institutes · TWTaipei Medical University · TW

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

introductionAtherosclerotic complications represent the leading cause of cardiovascular mortality globally. Dysfunction of endothelial cells (ECs) often initiates the pathological events in atherosclerosis.

objectivesIn this study, we sought to investigate the transcriptional profile of atherosclerotic aortae, identify novel regulator in dysfunctional ECs and hence provide mechanistic insights into atherosclerotic progression.

methodsWe applied single-cell RNA sequencing (scRNA-seq) on aortic cells from Western diet-fed apolipoprotein E-deficient (ApoE

resultsAmong the compendium of aortic cells, mesenchymal markers in ECs were significantly enriched. Two EC subsets were subsequently distinguished, as the 'endothelial-like' and 'mesenchymal-like' subsets. Conventional assays consistently identified SOX4 as a novel atherosclerotic marker in mouse and different human arteries, additional to a cancer marker. EC-specific SOX4 overexpression promoted atherogenesis and endothelial-to-mesenchymal transition (EndoMT). Importantly, hyperlipidemia-associated cytokines and oscillatory blood flow upregulated, whereas the anti-diabetic drug metformin pharmacologically suppressed SOX4 level in ECs.

conclusionOur study unravels SOX4 as a novel phenotypic regulator during endothelial dysfunction, which exacerbates atherogenesis. Our study also pinpoints hyperlipidemia-associated cytokines and oscillatory blood flow as endogenous SOX4 inducers, providing more therapeutic insights against atherosclerotic diseases.

Indexed as

AtherosclerosisEndothelial CellsAnimalsAortaCytokinesHumansMiceSingle-Cell AnalysisSOXC Transcription FactorsCytokinesSOX4 protein, humanSOXC Transcription FactorsAtherosclerosisEndoMTEndothelial cellsShear stressSingle-cell RNA sequencing

Identifiers

PMID36585108
PMCPMC9811326
OpenAlexW4214697101

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.