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Platelet Activation and Prothrombotic Factors for Atherosclerosis

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A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Endocrinology and Metabolism".

Deadline for manuscript submissions: closed (30 April 2022) | Viewed by 11508

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Special Issue Editor

Prof. Yuji Hirowatari

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Guest Editor

Department of Health Sciences, Saitama Prefectural University, Koshigaya, Japan
Interests: lipoprotein; vitamin E; platelets; serotonin; atherosclerosis; metabolic syndrome

Special Issue Information

Dear Colleagues,

Proinflammatory and prothrombotic factors can induce endothelial dysfunction and atherosclerotic plaque formation and progression. The activation of platelets induces an increase in proinflammatory and prothrombotic factors, by contact with monocytes/macrophages and neutrophils. Platelet–leukocyte crosstalk regulates leukocyte recruitment, the proliferation and differentiation of leukocytes, and the production of proinflammatory factors such as cytokines. The crosstalk between platelets and leukocytes may play a crucial role in atherogenesis; however, the underlying mechanisms remain unknown. This Special Issue will feature the contributions of platelet activation/prothrombotic factors showing platelet–leukocyte crosstalk to atherosclerosis.

It is currently very difficult to prove platelet activation. Focusing on the fact that activated platelets release serotonin, we have developed a highly accurate serotonin measurement system. Using the system, we found a significant association between plasma serotonin levels and atherosclerotic progression in type 2 diabetic patients. We would like to introduce our exciting results. We also welcome the submission of original articles, review articles, communications and letters on platelet–leukocyte crosstalk. I would like to make the Special Issue “Platelet Activation and Prothrombotic Factors for Atherosclerosis” great with your enormous help.

Prof. Yuji Hirowatari
Guest Editor

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

Platelet activation
Prothrombotic factors
Atherosclerosis
Inflammatory
Endothelial dysfunction
Macrophage

Published Papers (3 papers)

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Research

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9 pages, 1314 KiB

Open AccessArticle

Protease-Activated Receptor 1 in Human Carotid Atheroma Is Significantly Related to Iron Metabolism, Plaque Vulnerability, and the Patient’s Age

by Wei Li, Ehab Osman, Claes Forssell and Xi-Ming Yuan

Int. J. Mol. Sci. 2022, 23(12), 6363; https://doi.org/10.3390/ijms23126363 - 07 Jun 2022

Cited by 1 | Viewed by 1952

Abstract

(1) Background: Protease-activated receptor 1 (PAR1) has regulatory functions in inflammation, atherogenesis, and atherothrombosis. Chronic iron administration accelerates arterial thrombosis. Intraplaque hemorrhage and hemoglobin catabolism by macrophages are associated with dysregulated iron metabolism and atherosclerotic lesion instability. However, it remains unknown whether expressions of PAR1 in human atherosclerotic lesions are related to plaque severity, accumulation of macrophages, and iron-related proteins. We investigated the expression of PAR1 and its relation to the expression of ferritin and transferrin receptors in human carotid atherosclerotic plaques and then explored potential connections between their expressions, plaque development, and classical risk factors. (2) Methods: Carotid samples from 39 patients (25 males and 14 females) were immunostained with PAR1, macrophages, ferritin, and transferrin receptor. Double immunocytochemistry of PAR1 and ferritin was performed on THP-1 macrophages exposed to iron. (3) Results: PAR1 expression significantly increases with the patient’s age and the progression of human atherosclerotic plaques. Expressions of PAR1 are significantly correlated with the accumulation of CD68-positive macrophages, ferritin, and transferrin receptor 1 (TfR1), and inversely correlated with levels of high-density lipoprotein. In vitro, PAR1 is significantly increased in macrophages exposed to iron, and the expression of PAR1 is colocalized with ferritin expression. (4) Conclusions: PAR1 is significantly related to the progression of human atherosclerotic lesions and the patient’s age. PAR1 is also associated with macrophage infiltration and accumulation of iron metabolic proteins in human atherosclerotic lesions. Cellular iron-mediated induction of PAR1 and its colocalization with ferritin in macrophages may further indicate an important role of cellular iron in atherothrombosis. Full article

(This article belongs to the Special Issue Platelet Activation and Prothrombotic Factors for Atherosclerosis)

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Review

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20 pages, 2569 KiB

Open AccessReview

Fibrinogen and Atherosclerotic Cardiovascular Diseases—Review of the Literature and Clinical Studies

by Stanisław Surma and Maciej Banach

Int. J. Mol. Sci. 2022, 23(1), 193; https://doi.org/10.3390/ijms23010193 - 24 Dec 2021

Cited by 41 | Viewed by 5361

Abstract

Atherosclerotic cardiovascular diseases (ASCVD), including coronary artery disease, cerebrovascular disease, and peripheral arterial disease, represent a significant cause of premature death worldwide. Biomarkers, the evaluation of which would allow the detection of ASCVD at the earliest stage of development, are intensively sought. Moreover, from a clinical point of view, a valuable biomarker should also enable the assessment of the patient’s prognosis. It has been known for many years that the concentration of fibrinogen in plasma increases, inter alia, in patients with ASCVD. On the one hand, an increased plasma fibrinogen concentration may be the cause of the development of atherosclerotic lesions (increased risk of atherothrombosis); on the other hand, it may be a biomarker of ASCVD, as it is an acute phase protein. In addition, a number of genetic polymorphisms and post-translational modifications of fibrinogen were demonstrated that may contribute to the risk of ASCVD. This review summarizes the current data on the importance of fibrinogen as a biomarker of ASCVD, and also presents the relationship between molecular modifications of this protein in the context of ASCVD. Full article

(This article belongs to the Special Issue Platelet Activation and Prothrombotic Factors for Atherosclerosis)

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20 pages, 981 KiB

Open AccessReview

Inflammatory Mediators of Platelet Activation: Focus on Atherosclerosis and COVID-19

by Panagiotis Theofilis, Marios Sagris, Alexios S. Antonopoulos, Evangelos Oikonomou, Costas Tsioufis and Dimitris Tousoulis

Int. J. Mol. Sci. 2021, 22(20), 11170; https://doi.org/10.3390/ijms222011170 - 16 Oct 2021

Cited by 34 | Viewed by 3618

Abstract

Background: Atherosclerotic cardiovascular diseases are characterized by a dysregulated inflammatory and thrombotic state, leading to devastating complications with increased morbidity and mortality rates. Summary: In this review article, we present the available evidence regarding the impact of inflammation on platelet activation in atherosclerosis. Key messages: In the context of a dysfunctional vascular endothelium, structural alterations by means of endothelial glycocalyx thinning or functional modifications through impaired NO bioavailability and increased levels of von Willebrand factor result in platelet activation. Moreover, neutrophil-derived mediators, as well as neutrophil extracellular traps formation, have been implicated in the process of platelet activation and platelet-leukocyte aggregation. The role of pro-inflammatory cytokines is also critical since their receptors are also situated in platelets while TNF-α has also been found to induce inflammatory, metabolic, and bone marrow changes. Additionally, important progress has been made towards novel concepts of the interaction between inflammation and platelet activation, such as the toll-like receptors, myeloperoxidase, and platelet factor-4. The accumulating evidence is especially important in the era of the coronavirus disease-19 pandemic, characterized by an excessive inflammatory burden leading to thrombotic complications, partially mediated by platelet activation. Lastly, recent advances in anti-inflammatory therapies point towards an anti-thrombotic effect secondary to diminished platelet activation. Full article

(This article belongs to the Special Issue Platelet Activation and Prothrombotic Factors for Atherosclerosis)

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