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Biomedicines
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Platelets in Health and Disease: From Molecular Mechanisms to Therapeutic...
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Platelets in Health and Disease: From Molecular Mechanisms to Therapeutic Potential

A special issue of Biomedicines (ISSN 2227-9059). This special issue belongs to the section "Cell Biology and Pathology".

Deadline for manuscript submissions: closed (31 August 2025) | Viewed by 4616

Special Issue Editor

Dr. Henry Nording

E-Mail Website
Guest Editor
1. Cardioimmunology Group, Medical Clinic II, University Heart Center Luebeck, Luebeck, Germany
2. DZHK (German Research Centre for Cardiovascular Research), Partner Site Hamburg/Lübeck/Kiel, 23562 Lübeck, Germany
Interests: immunology; cardiology; vascular biology

Special Issue Information

Dear Colleagues,

Platelets are remarkably versatile cells, widely recognized for their central role in primary hemostasis. Their significance as key targets for pharmacological therapy in both primary and secondary prevention, as well as after vascular interventions involving the implantation of exogenous materials into the bloodstream, is well established. Moreover, the involvement of platelets in atherosclerosis is undisputed.

Recently, platelets have also been implicated in various tissue remodeling processes, such as apoptosis, immune patrolling, and adaptive immunity. They play a critical role in the immediate response to vascular injury by promoting vascular inflammation and immunomodulation. These discoveries have led to a broader understanding of platelets as immune cells.

Platelets continue to captivate both clinicians and basic scientists as new interactions between platelets, their precursor cells (megakaryocytes), and novel immune cell populations are uncovered. Emerging roles of platelets in disease mechanisms are being identified, and they are increasingly recognized as valuable targets for therapeutic interventions and as potential biomarkers.

Contributions to this Special Issue, "Platelets in Health and Disease: From Molecular Mechanisms to Therapeutic Potential", should focus on recent advancements that reinforce the concept of platelets as crucial mediators of vascular immunity, integral components of the immune system, promising therapeutic targets, or biomarkers, particularly in relation to their lipidome, transcriptome, or proteome.

Dr. Henry Nording
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. Biomedicines is an international peer-reviewed open access monthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2600 CHF (Swiss Francs). 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 biology
  • vascular immunity
  • atherosclerosis
  • therapeutic targets
  • biomarkers

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Published Papers (3 papers)

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Research

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15 pages, 2993 KB  
Article
Cold vs. Room Temperature: A Comparative Analysis of Platelet Functionality in Cold Storage
by Panagiotis V. Drossos, Sotirios P. Fortis, Alkmini T. Anastasiadi, Efthymia G. Pavlou, Andreas G. Tsantes, Gerasimos A. Spyratos, Effie G. Papageorgiou, Efrosyni G. Nomikou, Konstantinos E. Stamoulis, Georgios Dryllis, Vassilis L. Tzounakas, Marianna Politou, Serena Valsami and Anastasios G. Kriebardis
Biomedicines 2025, 13(2), 310; https://doi.org/10.3390/biomedicines13020310 - 27 Jan 2025
Cited by 4 | Viewed by 2565
Abstract
Background: The platelet functionality of cold-stored platelets remains a subject of debate. Our aim was to investigate the effect of temperature on the hemostatic properties of stored platelets. Methods: Ten split pooled platelets stored at cold and at room temperature were evaluated in [...] Read more.
Background: The platelet functionality of cold-stored platelets remains a subject of debate. Our aim was to investigate the effect of temperature on the hemostatic properties of stored platelets. Methods: Ten split pooled platelets stored at cold and at room temperature were evaluated in vitro on storage days 1, 5, 10, and 15 for metabolic, physiological, and vesiculation parameters, as well as their hemostatic profile using rotational thromboelastometry (ROTEM®). Results: The integrity profile was better preserved in the cold-stored platelets, as lower lactate dehydrogenase levels were documented (e.g., day 10: 261 ± 46 vs. 572 ± 220 U/L, 4 vs. 22 °C, p = 0.004). A time-dependent decrease in hemostatic capacity was evident regardless of the temperature, but the cold-stored units were linked to shorter clot initiation times and increased elasticity, strength, and firmness parameters, especially during extended storage (e.g., maximum clot firmness, INTEM day 15: 81 ± 2 vs. 19 ± 4 mm, 4 vs. 22 °C, p = 0.0008). Additionally, the aggregation of cold-stored platelets was superior after the addition of any agonist tested. Regarding vesiculation parameters, the extracellular vesicles of the units at 4 °C were characterized by a larger size from day 10 onwards, when they also presented higher procoagulant activity (e.g., phospholipid-dependent clotting time of day 15: 21.4 ± 2.3 vs. 25.0 ± 3.0 s, 4 vs. 22 °C, p = 0.016). Conclusion: Our results indicate that cold-stored platelets perform better than those stored at room temperature, demonstrating superior clot formation and stability. This suggests that cold storage may more effectively preserve platelet function, potentially offering advantages for transfusion therapy and the extension of shelf-life. However, the clinical relevance of these findings requires further investigation. Full article
(This article belongs to the Special Issue Platelets in Health and Disease: From Molecular Mechanisms to Therapeutic Potential)
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12 pages, 1321 KB  
Article
TRAP-Induced Platelet Reactivity Is Inhibited by Omega-3 Fatty Acid-Derived Prostaglandin E3 (PGE3)
by José-Miguel Osete, Faustino García-Candel, Francisco-José Fernández-Gómez, Miguel Blanquer, Noemí M. Atucha, Joaquín García-Estañ and David Iyú
Biomedicines 2024, 12(12), 2855; https://doi.org/10.3390/biomedicines12122855 - 16 Dec 2024
Viewed by 1399
Abstract
Background: Prostaglandins are naturally occurring local mediators that can participate in the modulation of the cardiovascular system through their interaction with Gs/Gi-coupled receptors in different tissues and cells, including platelets. Thrombin is one of the most important factors that regulates platelet reactivity and [...] Read more.
Background: Prostaglandins are naturally occurring local mediators that can participate in the modulation of the cardiovascular system through their interaction with Gs/Gi-coupled receptors in different tissues and cells, including platelets. Thrombin is one of the most important factors that regulates platelet reactivity and coagulation. Clinical trials have consistently shown that omega-3 fatty acid supplementation lowers the risk for cardiovascular mortality and morbidity. Since omega-3 fatty acids are the main precursors of PGE3 in vivo, it would be relevant to investigate the effects of PGE3 on Thrombin Receptor Activating Peptide (TRAP-6)-induced platelet reactivity to determine the receptors and possible mechanisms of action of these compounds. Methods: We have measured platelet aggregation, P-selectin expression, and vasodilator-stimulated phosphoprotein (VASP) phosphorylation to evaluate platelet reactivity induced by TRAP-6 to determine the effects of PGE3 on platelet function. Results: We assessed the ability of DG-041, a selective prostanoid EP3 receptor antagonist, and of ONO-AE3-208, a selective prostanoid EP4 receptor antagonist, to modify the effects of PGE3. PGE3 inhibited TRAP-6-induced platelet aggregation and activation. This inhibition was enhanced in the presence of a Gi-coupled EP3 receptor antagonist and abolished in the presence of a Gs-coupled EP4 receptor antagonist. The effects of PGE3 were directly related to changes in cAMP, assessed by VASP phosphorylation. Conclusions: The general effects of PGE3 on human platelet reactivity are the consequence of a balance between activatory and inhibitory effects at receptors that have contrary effects on adenylate cyclase. These results indicate a potential mechanism by which omega-3 fatty acids underlie cardioprotective effects. Full article
(This article belongs to the Special Issue Platelets in Health and Disease: From Molecular Mechanisms to Therapeutic Potential)
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Review

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24 pages, 1568 KB  
Review
α-Actinin-1 in Megakaryocytes: Its Structure, Interacting Proteins and Implications for Thrombopoiesis
by Lanlan Wu, Zhiqun Song, Yulan Zhou, Jiansong Huang and Xiaoxia Huang
Biomedicines 2025, 13(10), 2479; https://doi.org/10.3390/biomedicines13102479 - 11 Oct 2025
Viewed by 198
Abstract
Mutations in the ACTN1 gene, which encodes the cytoskeletal protein α-actinin-1, have been implicated in the etiology of autosomal dominant congenital macrothrombocytopenia. α-Actinin-1 is a member of the spectrin superfamily and is essential for key physiological processes in megakaryocytes and platelets. The pathophysiological [...] Read more.
Mutations in the ACTN1 gene, which encodes the cytoskeletal protein α-actinin-1, have been implicated in the etiology of autosomal dominant congenital macrothrombocytopenia. α-Actinin-1 is a member of the spectrin superfamily and is essential for key physiological processes in megakaryocytes and platelets. The pathophysiological mechanisms by which α-actinin-1 mutations lead to macrothrombocytopenia have been attributed to alterations in actin organization, increased binding affinity of α-actinin-1 to actin filaments, and modulation of integrin αIIbβ3 signaling. In previous studies, we utilized megakaryocyte-specific α-actinin-1 knockout (PF4-ACTN1−/−) mice to explore the influence of α-actinin-1 on megakaryocyte and platelet function. Despite these efforts, the precise mechanisms remain inadequately understood. To advance our understanding and clarify the role of α-actinin-1 in thrombopoiesis, we first delineated the functions of α-actinin-1 in megakaryocytes and platelets, followed by a comprehensive overview of the proteins known to interact with α-actinin-1. As a pivotal scaffold protein, α-actinin-1 interacts with a complex network of partners, including integrin αIIbβ3, and actin filaments, to modulate cytoskeletal dynamics, megakaryocyte maturation, and proplatelet formation. In addition to its well-documented proteins that interact with α-actinin-1 within megakaryocytes and platelets, α-actinin-1 also associates with proteins outside the megakaryocytic lineage, such as cytohesin-2 and MOB1, which have been predominantly examined in other cellular contexts. These varied interactions imply that α-actinin-1 may influence megakaryocyte and platelet functions through multiple mechanisms. This review provides a comprehensive synthesis of current knowledge regarding the structure, binding partners of α-actinin-1, and essential roles of α-actinin-1 in thrombopoiesis. Full article
(This article belongs to the Special Issue Platelets in Health and Disease: From Molecular Mechanisms to Therapeutic Potential)
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