Evidence map›Paper›PMID 32867213›Full record

ArticleInternational journal of molecular sciences2020

Mitoquinone (MitoQ) Inhibits Platelet Activation Steps by Reducing ROS Levels.

Diego Méndez, Diego Arauna, Francisco Fuentes, Ramiro Araya-Maturana, Iván Palomo, Marcelo Alarcón, David Sebastián, Antonio Zorzano, Eduardo Fuentes

Open access · goldAbstract read
In one paragraph

Article in International journal of molecular sciences, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
3.3field-weighted citation impact, top 7% 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

25 citing papers in PubMed, 48 citations in OpenAlex.

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  16. Isorhamnetin: what is theFrontiers in pharmacology · 2024
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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

9 authors at 2 institutions in 2 countries.

Diego MéndezThrombosis Research Center, Medical Technology School, Department of Clinical Biochemistry and Immunohaematology, Faculty of Health Sciences, Universidad de Talca, Talca 3460000, Chile.ORCID 0000-0003-0156-2913
Diego AraunaThrombosis Research Center, Medical Technology School, Department of Clinical Biochemistry and Immunohaematology, Faculty of Health Sciences, Universidad de Talca, Talca 3460000, Chile.ORCID 0000-0001-7132-991X
Francisco FuentesEscuela de Medicina, Universidad de Talca, Talca 3460000, Chile.
Ramiro Araya-MaturanaInstituto de Química de Recursos Naturales, Universidad de Talca, Talca 3460000, Chile.ORCID 0000-0002-5082-9146
Iván PalomoThrombosis Research Center, Medical Technology School, Department of Clinical Biochemistry and Immunohaematology, Faculty of Health Sciences, Universidad de Talca, Talca 3460000, Chile.
Marcelo AlarcónThrombosis Research Center, Medical Technology School, Department of Clinical Biochemistry and Immunohaematology, Faculty of Health Sciences, Universidad de Talca, Talca 3460000, Chile.ORCID 0000-0001-7596-5382
David SebastiánInstitute for Research in Biomedicine (IRB Barcelona), The Barcelona Institute of Science and Technology, 08007 Barcelona, Spain.ORCID 0000-0002-7260-3869
Antonio ZorzanoInstitute for Research in Biomedicine (IRB Barcelona), The Barcelona Institute of Science and Technology, 08007 Barcelona, Spain.
Eduardo FuentesThrombosis Research Center, Medical Technology School, Department of Clinical Biochemistry and Immunohaematology, Faculty of Health Sciences, Universidad de Talca, Talca 3460000, Chile.ORCID 0000-0003-0099-4108
University of Talca · CLInstituto de Salud Carlos III · ES

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Platelet activation plays a key role in cardiovascular diseases. The generation of mitochondrial reactive oxygen species (ROS) has been described as a critical step required for platelet activation. For this reason, it is necessary to find new molecules with antiplatelet activity and identify their mechanisms of action. Mitoquinone (MitoQ) is a mitochondria-targeted antioxidant that reduces mitochondrial overproduction of ROS. In this work, the antiplatelet effect of MitoQ through platelet adhesion and spreading, secretion, and aggregation was evaluated. Thus MitoQ, in a non-toxic effect, decreased platelet adhesion and spreading on collagen surface, and expression of P-selectin and CD63, and inhibited platelet aggregation induced by collagen, convulxin, thrombin receptor activator peptide-6 (TRAP-6), and phorbol 12-myristate 13-acetate (PMA). As an antiplatelet mechanism, we showed that MitoQ produced mitochondrial depolarization and decreased ATP secretion. Additionally, in platelets stimulated with antimycin A and collagen MitoQ significantly decreased ROS production. Our findings showed, for the first time, an antiplatelet effect of MitoQ that is probably associated with its mitochondrial antioxidant effect.

Indexed as

Adenosine TriphosphateAnimalsAntioxidantsBlood PlateletsCells, CulturedCollagenHumansMiceMitochondriaOligopeptidesOrganophosphorus CompoundsPhorbol EstersPlatelet ActivationP-SelectinReactive Oxygen SpeciesTetraspanin 30Adenosine TriphosphateAntioxidantsCD63 protein, humanCollagenmitoquinoneOligopeptidesOrganophosphorus Compoundsphorbol-12-myristatePhorbol EstersP-SelectinReactive Oxygen SpeciesSer-Phe-Phe-Leu-Arg-AsnTetraspanin 30UbiquinonemitochondriaMitoQmitoquinoneplateletsROS

Identifiers

PMID32867213
PMCPMC7503844
OpenAlexW3080870978

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.