Evidence map›Paper›PMID 30590395›Full record

ReviewCardiovascular research2019

Circulating blood cells and extracellular vesicles in acute cardioprotection.

Sean M Davidson, Ioanna Andreadou, Lucio Barile, Yochai Birnbaum, Hector A Cabrera-Fuentes, Michael V Cohen, James M Downey, Henrique Girao, Pasquale Pagliaro, Claudia Penna and 3 more

Open access · bronzeAbstract readReview
In one paragraph

Review in Cardiovascular research, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 83 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
83citing papers in PubMed, 1 pooled it
6.1field-weighted citation impact, top 3% 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

83 citing papers in PubMed, 1 synthesis or guideline pooled it, 136 citations in OpenAlex.

  1. Pooled it
  2. Trial
  3. Trial
  4. Trial
  5. Review
  6. Article
  7. Article
  8. Article
  9. Review
  10. Review
  11. Extracellular vesicles in viral disease management.Current research in microbial sciences · 2026
    Review
  12. TargetingJournal of pharmaceutical analysis · 2025
    Article
  13. Article
  14. Quercetin is a potential therapy for post-infarction NETosis formation.Naunyn-Schmiedeberg's archives of pharmacology · 2025
    Article
  15. Article
  16. Article
  17. Review
  18. Article
  19. Article
  20. Article

23 more citing papers are in PubMed but not listed here.

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

13 authors at 11 institutions in 12 countries.

Sean M DavidsonThe Hatter Cardiovascular Institute, University College London, 67 Chenies Mews, London, UK.
Ioanna AndreadouLaboratory of Pharmacology, Faculty of Pharmacy, National and Kapodistrian University of Athens, Athens, Greece.
Lucio BarileCellular and Molecular Cardiology Laboratory, Cardiocentro Ticino Foundation and Swiss Institute for Regenerative Medicine (SIRM), Lugano, Switzerland.
Yochai BirnbaumSection of Cardiology, Department of Medicine, Baylor College of Medicine and The Texas Heart Institute, Baylor St. Luke Medical Center, MS BCM620, One Baylor Plaza, Houston, TX77030, USA.
Hector A Cabrera-FuentesCardiovascular and Metabolic Disorders Program, Duke-NUS Medical School, Singapore, Singapore.
Michael V CohenDepartment of Medicine, University of South Alabama, College of Medicine, Mobile, AL, USA.
James M DowneyDepartment of Physiology and Cell Biology, University of South Alabama, College of Medicine, Mobile, AL, USA.
Henrique GiraoCoimbra Institute for Clinical and Biomedical Research (iCBR), Faculty of Medicine, University of Coimbra, Coimbra, Portugal.
Pasquale PagliaroDepartment of Biological and Clinical Sciences, University of Turin, Torino, Italy.
Claudia PennaDepartment of Biological and Clinical Sciences, University of Turin, Torino, Italy.
John PernowDivision of Cardiology, Department of Medicine, Karolinska Institutet, Karolinska University Hospital, Stockholm, Sweden.
Klaus T PreissnerDepartment of Biochemistry, Medical School, Justus-Liebig-University, Giessen, Germany.
Péter FerdinandyDepartment of Pharmacology and Pharmacotherapy, Semmelweis University, Nagyvárad tér 4, Budapest 1089, Hungary.
University of South Alabama · USUniversity of Turin · ITBaylor College of Medicine · USKarolinska University Hospital · SENational and Kapodistrian University of Athens · GRNational Heart Centre Singapore · SGSemmelweis University · HUSwiss Institute for Regenerative Medicine · CHUniversity College London · GBUniversity of Coimbra · PTUniversity of Giessen · DE

Funding

British Heart Foundation PG/16/85/32471British Heart Foundation PG/18/44/33790Department of HealthMedical Research Council G0700933Medical Research Council MR/K002066/1
6 · The paper itself

Abstract

During an ST-elevation myocardial infarction (STEMI), the myocardium undergoes a prolonged period of ischaemia. Reperfusion therapy is essential to minimize cardiac injury but can paradoxically cause further damage. Experimental procedures to limit ischaemia and reperfusion (IR) injury have tended to focus on the cardiomyocytes since they are crucial for cardiac function. However, there is increasing evidence that non-cardiomyocyte resident cells in the heart (as discussed in a separate review in this Spotlight series) as well as circulating cells and factors play important roles in this pathology. For example, erythrocytes, in addition to their main oxygen-ferrying role, can protect the heart from IR injury via the export of nitric oxide bioactivity. Platelets are well-known to be involved in haemostasis and thrombosis, but beyond these roles, they secrete numerous factors including sphingosine-1 phosphate (S1P), platelet activating factor, and cytokines that can all strongly influence the development of IR injury. This is particularly relevant given that most STEMI patients receive at least one type of platelet inhibitor. Moreover, there are large numbers of circulating vesicles in the blood, including microvesicles and exosomes, which can exert both beneficial and detrimental effects on IR injury. Some of these effects are mediated by the transfer of microRNA (miRNA) to the heart. Synthetic miRNA molecules may offer an alternative approach to limiting the response to IR injury. We discuss these and other circulating factors, focussing on potential therapeutic targets relevant to IR injury. Given the prevalence of comorbidities such as diabetes in the target patient population, their influence will also be discussed. This article is part of a Cardiovascular Research Spotlight Issue entitled 'Cardioprotection Beyond the Cardiomyocyte', and emerged as part of the discussions of the European Union (EU)-CARDIOPROTECTION Cooperation in Science and Technology (COST) Action, CA16225.

Indexed as

AnimalsBlood PlateletsCirculating MicroRNAErythrocytesExtracellular VesiclesHemostasisHumansMyocardial Reperfusion InjuryMyocardiumPlatelet Aggregation InhibitorsSignal TransductionST Elevation Myocardial InfarctionCirculating MicroRNAPlatelet Aggregation InhibitorsCardioprotectionExosomesHaematopoietic cellsIschaemiaReperfusion

Identifiers

PMID30590395
PMCPMC6529916
OpenAlexW2906459748

What OpenQuestion holds

Textmetadata
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.