Evidence map›Paper›PMID 34185408›Full record

ArticleClinical and translational medicine2021

Integrative multiomics analysis of human atherosclerosis reveals a serum response factor-driven network associated with intraplaque hemorrhage.

Han Jin, Pieter Goossens, Peter Juhasz, Wouter Eijgelaar, Marco Manca, Joël M H Karel, Evgueni Smirnov, Cornelis J J M Sikkink, Barend M E Mees, Olivia Waring and 10 more

Open access · goldAbstract read
In one paragraph

Article in Clinical and translational medicine, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers.

0numbers the graph read from it
0cells of the map it votes in
47citing papers in PubMed
7.5field-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

47 citing papers in PubMed, 95 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 7 institutions in 5 countries.

Han JinDepartment of Pathology, School for Cardiovascular Diseases (CARIM), Maastricht UMC+, Maastricht, The Netherlands.ORCID 0000-0002-0955-6289
Pieter GoossensDepartment of Pathology, School for Cardiovascular Diseases (CARIM), Maastricht UMC+, Maastricht, The Netherlands.ORCID 0000-0002-7269-6372
Peter JuhaszPJ Consulting, Natick, Massachusetts, USA.ORCID 0000-0002-4637-795X
Wouter EijgelaarDepartment of Pathology, School for Cardiovascular Diseases (CARIM), Maastricht UMC+, Maastricht, The Netherlands.ORCID 0000-0001-8690-1843
Marco MancaDepartment of Pathology, School for Cardiovascular Diseases (CARIM), Maastricht UMC+, Maastricht, The Netherlands.ORCID 0000-0002-7869-2620
Joël M H KarelDepartment of Data Science and Knowledge Engineering, Maastricht University, Maastricht, The Netherlands.ORCID 0000-0001-6209-3589
Evgueni SmirnovDepartment of Data Science and Knowledge Engineering, Maastricht University, Maastricht, The Netherlands.ORCID 0000-0003-2778-6042
Cornelis J J M SikkinkDepartment of Vascular Surgery, Zuyderland Medical Centre, Heerlen, The Netherlands.ORCID 0000-0002-8110-3575
Barend M E MeesDepartment of Surgery, Maastricht UMC+, Maastricht, The Netherlands.ORCID 0000-0001-6545-5813
Olivia WaringDepartment of Pathology, School for Cardiovascular Diseases (CARIM), Maastricht UMC+, Maastricht, The Netherlands.ORCID 0000-0002-5786-8121
Kim van KuijkDepartment of Pathology, School for Cardiovascular Diseases (CARIM), Maastricht UMC+, Maastricht, The Netherlands.ORCID 0000-0001-8880-9039
Gregorio E FazziDepartment of Pathology, School for Cardiovascular Diseases (CARIM), Maastricht UMC+, Maastricht, The Netherlands.ORCID 0000-0001-7068-8435
Marion J J GijbelsDepartment of Pathology, School for Cardiovascular Diseases (CARIM), Maastricht UMC+, Maastricht, The Netherlands.ORCID 0000-0002-4906-0384
Martina KutmonDepartment of Bioinformatics (BiGCaT), Maastricht Centre for Systems Biology (MaCSBio), Maastricht University, Maastricht, The Netherlands.ORCID 0000-0002-7699-8191
Chris T A EveloDepartment of Bioinformatics (BiGCaT), Maastricht Centre for Systems Biology (MaCSBio), Maastricht University, Maastricht, The Netherlands.ORCID 0000-0002-5301-3142
Ulf HedinDepartment of Molecular Medicine and Surgery, Karolinska Institute, Solna, Sweden.ORCID 0000-0001-9212-3945
Mat J A P DaemenDepartment of Pathology, Amsterdam Cardiovascular Sciences, Amsterdam UMC, Amsterdam, The Netherlands.ORCID 0000-0003-1076-199X
Judith C SluimerDepartment of Pathology, School for Cardiovascular Diseases (CARIM), Maastricht UMC+, Maastricht, The Netherlands.ORCID 0000-0002-0269-4582
Ljubica MaticDepartment of Molecular Medicine and Surgery, Karolinska Institute, Solna, Sweden.ORCID 0000-0002-7294-9667
Erik A L BiessenDepartment of Pathology, School for Cardiovascular Diseases (CARIM), Maastricht UMC+, Maastricht, The Netherlands.ORCID 0000-0002-6454-8548
Maastricht University Medical Centre · NLKarolinska Institutet · SEMaastricht School of Management · NLMaastricht University · NLAmsterdam Neuroscience · NLCombat Capabilities Development Command Soldier Center · USZuyderland Medisch Centrum · NL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundWhile single-omics analyses on human atherosclerotic plaque have been very useful to map stage- or disease-related differences in expression, they only partly capture the array of changes in this tissue and suffer from scale-intrinsic limitations. In order to better identify processes associated with intraplaque hemorrhage and plaque instability, we therefore combined multiple omics into an integrated model.

methodsIn this study, we compared protein and gene makeup of low- versus high-risk atherosclerotic lesion segments from carotid endarterectomy patients, as judged from the absence or presence of intraplaque hemorrhage, respectively. Transcriptomic, proteomic, and peptidomic data of this plaque cohort were aggregated and analyzed by DIABLO, an integrative multivariate classification and feature selection method.

resultsWe identified a protein-gene associated multiomics model able to segregate stable, nonhemorrhaged from vulnerable, hemorrhaged lesions at high predictive performance (AUC >0.95). The dominant component of this model correlated with αSMA

conclusionsIn conclusion, our integrative omics study has identified an intraplaque hemorrhage-associated cardiovascular signature that provides excellent stratification of low- from high-risk carotid artery plaques in several independent cohorts. Further study revealed suppression of an SRF-regulated disease network, controlling lesion stability, in vulnerable plaque, which can serve as a scaffold for the design of targeted intervention in plaque destabilization.

Indexed as

Gene Regulatory NetworksTranscriptomeAtherosclerosisBiomarkersGene Expression RegulationHumansMalePeptidesPrognosisProteomeSerum Response FactorBiomarkersPeptidesProteomeSerum Response FactorSRF protein, humancarotid atherosclerosismultiomics integrationproteomicstranscriptomics

Identifiers

PMID34185408
PMCPMC8236116
OpenAlexW3174687343

What OpenQuestion holds

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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.