ijms-logo

Journal Browser

Journal Browser

Molecular Basis of Platelet Function in Thrombosis and Beyond

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Pathology, Diagnostics, and Therapeutics".

Deadline for manuscript submissions: closed (31 December 2020) | Viewed by 4662

Special Issue Editors


E-Mail Website
Guest Editor
Head of the Laboratory of Cardiology, GIGA‐Cardiovascular Sciences, University of Liège, CHU Sart‐Tilman Liège, Belgium
Interests: platelets; thrombosis; hemostasis; platelet-neutrophil interactions; bacterial infection; inflammation; valvular heart disease; aortic stenosis; prosthetic heart valves; transcatheter aortic valve implantation; cardiovascular devices

E-Mail Website
Guest Editor
Pôle de Recherche Cardiovasculaire (CARD), Institut de Recherche Expérimentale et Clinique (IREC), Université Catholique de Louvain (UCLouvain), 1200 Brussels, Belgium
Interests: platelets; metabolism; AMPK signaling; thrombosis; myocardial infarction; ventricular remodeling; fibrosis; cardiac fibroblast biology; endothelial barrier; stent; mouse models; translational research
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Circulating platelets and coagulation play a crucial role in hemostasis, acting to maintain the integrity of a closed circulatory system after blood vessel injury. Under physiological conditions, regulatory mechanisms restrain thrombus formation. When pathologic processes disturb these mechanisms, thrombosis can occur either in the arterial or in the venous circulation with tremendous impact on human health. Thrombosis is the cause of ischemic heart disease, ischemic stroke, and venous thromboembolism, which account for one in four deaths worldwide. Antiplatelet agents have proven efficacy to prevent thrombosis in patients with coronary artery disease or peripheral vascular diseases.

Beyond thrombosis, platelets also contribute to other various biological processes including inflammation, infection, immunity, and cancer. They may also be involved in calcifying or fibrotic diseases. There is therefore a growing interest in assessing whether platelets could be targeted or whether they could represent new biomarkers of initiation, evolution, or outcome in other pathologies than thrombosis.

This Special Issue is dedicated to the identification and description of platelet-related molecular mechanisms underlying not only thrombosis but also other systemic or cardiovascular pathologies, such as acute or chronic inflammatory diseases, cancer, valvular heart diseases, or heart failure. The objective is to highlight potential molecular interventions to prevent or treat theses pathologies towards a molecular medicine perspective.

Dr. Sandrine Horman
Dr. Oury Cécile
Guest Editors

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. International Journal of Molecular Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. There is an Article Processing Charge (APC) for publication in this open access journal. For details about the APC please see here. Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • platelets 
  • thrombosis 
  • inflammation 
  • infection 
  • cancer 
  • calcification 
  • fibrosis 
  • molecular pathology

Published Papers (1 paper)

Order results
Result details
Select all
Export citation of selected articles as:

Research

12 pages, 1508 KiB  
Article
Mitoquinone (MitoQ) Inhibits Platelet Activation Steps by Reducing ROS Levels
by Diego Méndez, Diego Arauna, Francisco Fuentes, Ramiro Araya-Maturana, Iván Palomo, Marcelo Alarcón, David Sebastián, Antonio Zorzano and Eduardo Fuentes
Int. J. Mol. Sci. 2020, 21(17), 6192; https://doi.org/10.3390/ijms21176192 - 27 Aug 2020
Cited by 24 | Viewed by 4356
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 [...] Read more.
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. Full article
(This article belongs to the Special Issue Molecular Basis of Platelet Function in Thrombosis and Beyond)
Show Figures

Figure 1

Back to TopTop