Evidence map›Paper›PMID 39387619›Full record

ArticleThe FEBS journal2024

Hemin-induced platelet activation is regulated by the ACKR3 chemokine surface receptor and has implications for passivation of vulnerable atherosclerotic plaques.

Zoi Laspa, Valerie Dicenta-Baunach, David Schaale, Manuel Sigle, Ravi Hochuli, Tatsiana Castor, Alp Bayrak, Tobias Harm, Karin Anne Lydia Müller, Thanigaimalai Pillaiyar and 3 more

Abstract read
In one paragraph

Article in The FEBS journal, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
–field-weighted citation impact
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

3 citing papers in PubMed.

  1. Haemolytic injury and cardiovascular disease.Nature reviews. Cardiology · 2026
    Review
  2. Receptor-Dependent and -Independent Effects of Hemin on Platelet Plasma Membrane Disintegration.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026
    Article
  3. Article
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.

Zoi LaspaDepartment of Cardiology and Angiology, University Hospital Tübingen, University Tübingen, Germany.
Valerie Dicenta-BaunachDepartment of Cardiology and Angiology, University Hospital Tübingen, University Tübingen, Germany.
David SchaaleDepartment of Cardiology and Angiology, University Hospital Tübingen, University Tübingen, Germany.
Manuel SigleDepartment of Cardiology and Angiology, University Hospital Tübingen, University Tübingen, Germany.
Ravi HochuliDepartment of Cardiology and Angiology, University Hospital Tübingen, University Tübingen, Germany.
Tatsiana CastorDepartment of Cardiology and Angiology, University Hospital Tübingen, University Tübingen, Germany.
Alp BayrakDepartment of Pharmaceutical and Medicinal Chemistry, Institute of Pharmaceutical Sciences, University Tübingen, Germany.
Tobias HarmDepartment of Cardiology and Angiology, University Hospital Tübingen, University Tübingen, Germany.
Karin Anne Lydia MüllerDepartment of Cardiology and Angiology, University Hospital Tübingen, University Tübingen, Germany.
Thanigaimalai PillaiyarDepartment of Pharmaceutical and Medicinal Chemistry, Institute of Pharmaceutical Sciences, University Tübingen, Germany.
Stefan LauferDepartment of Pharmaceutical and Medicinal Chemistry, Institute of Pharmaceutical Sciences, University Tübingen, Germany.
Anne-Katrin RohlfingDepartment of Cardiology and Angiology, University Hospital Tübingen, University Tübingen, Germany.
Meinrad Paul GawazDepartment of Cardiology and Angiology, University Hospital Tübingen, University Tübingen, Germany.ORCID 0000-0003-1124-9592

Funding

Deutsche Forschungsgemeinschaft 335549539Deutsche Gesellschaft für Kardiologie-Herz und Kreislaufforschung
6 · The paper itself

Abstract

In vulnerable atherosclerotic plaques, intraplaque hemorrhages (IPH) result in hemolysis of red blood cells and release of hemoglobin and free hemin. Hemin activates platelets and leads to thrombosis. Agonism of the inhibitory platelet receptor ACKR3 inhibits hemin-dependent platelet activation and thrombus formation. To characterize the effect of hemin and ACKR3 agonism on isolated human platelets, multi-color flow cytometry and classical experimental setup such as light transmission aggregometry and a flow chamber assay were used. Hemin induces platelet aggregation and ex vivo platelet-dependent thrombus formation on immobilized collagen under a low shear rate of 500 s

Indexed as

Blood PlateletsHeminPlaque, AtheroscleroticPlatelet ActivationPlatelet AggregationHumansReceptors, CXCRThrombosisACKR3 protein, humanHeminReceptors, CXCRACKR3heminintraplaque hemorrhage (IPH)multi‐color flow cytometryplatelets

Identifiers

PMID39387619
PMCPMC11653686

What OpenQuestion holds

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LicenceCC BY
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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.