Evidence map›Paper›PMID 35494231›Full record

ArticleiScience2022

Clinical risk scores for stroke correlate with molecular signatures of vulnerability in symptomatic carotid patients.

Katarina Wadén, Eva Karlöf, Sampath Narayanan, Mariette Lengquist, Göran K Hansson, Ulf Hedin, Joy Roy, Ljubica Matic

Open access · goldAbstract read
In one paragraph

Article in iScience, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed, 1 pooled it
1.4field-weighted citation impact, top 21% 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

10 citing papers in PubMed, 1 synthesis or guideline pooled it, 10 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
  4. Article
  5. A RareJournal of clinical medicine · 2025
    Article
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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

8 authors at 1 institution in 1 country.

Katarina WadénVascular Surgery, Department of Molecular Medicine and Surgery, Karolinska Institutet and Karolinska University Hospital, 17176 Stockholm, Sweden.
Eva KarlöfVascular Surgery, Department of Molecular Medicine and Surgery, Karolinska Institutet and Karolinska University Hospital, 17176 Stockholm, Sweden.
Sampath NarayananVascular Surgery, Department of Molecular Medicine and Surgery, Karolinska Institutet and Karolinska University Hospital, 17176 Stockholm, Sweden.
Mariette LengquistVascular Surgery, Department of Molecular Medicine and Surgery, Karolinska Institutet and Karolinska University Hospital, 17176 Stockholm, Sweden.
Göran K HanssonCardiovascular Medicine Unit, Department of Medicine, Center for Molecular Medicine, Karolinska Institutet and Karolinska University Hospital, 17176 Stockholm, Sweden.
Ulf HedinVascular Surgery, Department of Molecular Medicine and Surgery, Karolinska Institutet and Karolinska University Hospital, 17176 Stockholm, Sweden.
Joy RoyVascular Surgery, Department of Molecular Medicine and Surgery, Karolinska Institutet and Karolinska University Hospital, 17176 Stockholm, Sweden.
Ljubica MaticVascular Surgery, Department of Molecular Medicine and Surgery, Karolinska Institutet and Karolinska University Hospital, 17176 Stockholm, Sweden.
Karolinska University Hospital · SE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Unstable carotid stenosis is an important cause of ischemic stroke, yet the basis of disease pathophysiology remains largely unknown. We hypothesized that integrated analyses of symptomatic carotid stenosis patients at increased stroke risk stratified by clinical scores, CAR and ABCD2, with transcriptomic and clinical data could improve identification of molecular pathways and targets for instability. We show that high CAR score reflects plaque instability processes related to intra-plaque hemorrhage, angiogenesis, inflammation, and foam cell differentiation, whereas ABCD2 associates with neutrophil-mediated immunity, foam cell differentiation, cholesterol transport, and coagulation. Repressed processes in plaques from high-risk patients were ossification, chondrocyte differentiation, SMC migration, and ECM organization.

Indexed as

Cell biologyHealth sciencesTranscriptomics

Identifiers

PMID35494231
PMCPMC9046225
OpenAlexW4224224123

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.