Evidence map›Paper›PMID 35850658›Full record

ArticleBMC cardiovascular disorders2022

Increased expression of miR-224-5p in circulating extracellular vesicles of patients with reduced coronary flow reserve.

Kreema James, Paulina Bryl-Gorecka, Björn Olde, Olof Gidlof, Kristina Torngren, David Erlinge

Open access · goldAbstract read
In one paragraph

Article in BMC cardiovascular disorders, 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
0.9field-weighted citation impact, top 29% 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. Trial
  3. Review
  4. Review
  5. Atrial Fibroblasts-Derived Extracellular Vesicles Exacerbate Atrial Arrhythmogenesis.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025
    Article
  6. Review
  7. Liquid Biopsy in the Clinical Management of Cancers.International journal of molecular sciences · 2024
    Review
  8. Article
  9. Review
  10. Review
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

6 authors at 1 institution in 1 country.

Kreema JamesDepartment of Cardiology, Clinical Sciences, Biomedical Centre, Faculty of Medicine, Lund University, D12, Sölvegatan 17, 22362, Lund, Sweden. kreema.james@med.lu.se.
Paulina Bryl-GoreckaDepartment of Cardiology, Clinical Sciences, Biomedical Centre, Faculty of Medicine, Lund University, D12, Sölvegatan 17, 22362, Lund, Sweden.
Björn OldeDepartment of Cardiology, Clinical Sciences, Biomedical Centre, Faculty of Medicine, Lund University, D12, Sölvegatan 17, 22362, Lund, Sweden.
Olof GidlofDepartment of Cardiology, Clinical Sciences, Biomedical Centre, Faculty of Medicine, Lund University, D12, Sölvegatan 17, 22362, Lund, Sweden.
Kristina TorngrenDepartment of Cardiology, Clinical Sciences, Biomedical Centre, Faculty of Medicine, Lund University, D12, Sölvegatan 17, 22362, Lund, Sweden.
David ErlingeDepartment of Cardiology, Clinical Sciences, Biomedical Centre, Faculty of Medicine, Lund University, D12, Sölvegatan 17, 22362, Lund, Sweden.
Lund University · SE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundEndothelial and microvascular dysfunction are pivotal causes of major adverse cardiac events predicted by coronary flow reserve (CFR). Extracellular Vesicles (EVs) have been studied extensively in the pathophysiology of coronary artery disease. However, little is known on the impact of the non-coding RNA content of EVs with respect to CFR.

methodsWe carried out a study among 120 patients divided by high-CFR and low-CFR to profile the miRNA content of circulating EVs.

resultsA multiplex array profiling on circulating EVs revealed mir-224-5p (p-value ≤ 0.000001) as the most differentially expressed miRNA in the Low-CFR group and showed a significantly independent relationship to CFR. Literature survey indicated the origin of the miR from liver cells and not of platelet, leukocyte, smooth muscle or endothelial (EC) origin. A q-PCR panel of the conventional cell type-EVs along with hepatic EVs showed that EVs from liver cells showed higher expression of the miR-224-5p. FACS analysis demonstrated the presence of liver-specific (ASGPR-1+/CD14-) EVs in the plasma of our cohort with the presence of Vanin-1 required to enter the EC barrier. Hepatic EVs with and without the miR-224-5p were introduced to ECs in-vitro, but with no difference in effect on ICAM-1 or eNOS expression. However, hepatic EVs elevated endothelial ICAM-1 levels per se independent of the miR-224-5p.

conclusionThis indicated a role of hepatic EVs identified by the miR-224-5p in endothelial dysfunction in patients with Low CFR.

Indexed as

Extracellular VesiclesMicroRNAsHumansIntercellular Adhesion Molecule-1LiverPlasmaIntercellular Adhesion Molecule-1MicroRNAsMIRN224 microRNA, humanCardiovascular diseaseCoronary flow reserveExtracellular vesiclesHepaticMajor adverse cardiac eventsMicro-RNA

Identifiers

PMID35850658
PMCPMC9290204
OpenAlexW4285726152

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.