Platelets in Human Health and Diseases

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

Deadline for manuscript submissions: 31 July 2026 | Viewed by 915

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Research and Education Unit for Experimental Biotechnology, Department of Transplantology and General Surgery, Faculty of Medicine, Collegium Medicum in Bydgoszcz, Nicolaus Copernicus University in Toruń, 85-094 Bydgoszcz, Poland
Interests: platelet; hemostasis; thrombosis; antiplatelet drugs; inflammation; cancer; cardiovascular diseases
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Dear Colleagues,

Platelets are tiny blood cells with several physiological purposes; they play a key role in both health and disease. In health, platelets circulate in the bloodstream and remain in a resting state until they are activated by injury or other stimuli. Maintaining the proper balance between thrombosis and bleeding is a dynamic process involving many pro- and anticoagulant components. At the site of vascular injury, platelet accumulation is the first wave of hemostasis. Platelet adhesion, activation, and aggregation are critical events in hemostasis. Many basic science projects and research studies are investigating novel pathophysiological mechanisms and providing new insights into the current understanding of the contribution of platelets to many clinical situations, such as inflammation, tissue regeneration, cancer progression, and other pathophysiological processes. In disease states, platelets can be involved in the progression and severity of conditions such as cardiovascular diseases, diabetes mellitus, and cancer.

Prof. Dr. Joanna Sikora
Guest Editor

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Keywords

  • platelet
  • hemostasis
  • thrombosis
  • antiplatelet drugs
  • inflammation
  • cancer
  • cardiovascular diseases

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Published Papers (2 papers)

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Research

17 pages, 2726 KB  
Article
Xanthium strumarium L. Exhibits Potent Antiplatelet and Antithrombotic Effects by Modulating MAPK and PI3K/AKT Signaling Pathways and Inhibiting Ferric Chloride-Induced Thrombosis
by Abdul Wahab Akram, Ga Hee Lee, Su-Min Baek, Jinsu Kang, Yoonhoi Koo, Yein Oh, Min-Soo Seo, Evelyn Saba, Dong-Ha Lee and Man Hee Rhee
Biomedicines 2025, 13(12), 2924; https://doi.org/10.3390/biomedicines13122924 - 28 Nov 2025
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Abstract
Background: Cardiovascular diseases, driven by platelet hyperactivation and thrombosis, remain the leading global cause of death. Excessive platelet activation contributes to atherosclerosis and thrombo-inflammatory disorders, underscoring the urgent need for safer and more effective antiplatelet agents. Objectives:Xanthium strumarium L. (X. strumarium [...] Read more.
Background: Cardiovascular diseases, driven by platelet hyperactivation and thrombosis, remain the leading global cause of death. Excessive platelet activation contributes to atherosclerosis and thrombo-inflammatory disorders, underscoring the urgent need for safer and more effective antiplatelet agents. Objectives:Xanthium strumarium L. (X. strumarium) has been reported to exhibit a wide range of pharmacological effects, including anti-inflammatory and antioxidant activities. However, its antiplatelet and antithrombotic effects remain unexplored. Therefore, the present study aimed to comprehensively evaluate the antiplatelet and antithrombotic effects of X. strumarium through integrated in vitro and in vivo experiments. Methods: The principal bioactive compounds present in the X. strumarium extract were identified through GC–MS analysis. In vitro antiplatelet effects were evaluated via light transmission aggregometry, scanning electron microscopy (SEM), ATP and calcium mobilization assays, αIIbβ3 binding assay, clot retraction assay, and Western blotting. In vivo ferric chloride-induced (FeCl3) murine thrombus model was established to evaluate thrombogenesis. Results: Our results demonstrated that X. strumarium at 25, 50, or 100 μg/mL significantly inhibited collagen, ADP, U46619, and thrombin-induced platelet aggregation. SEM revealed that X. strumarium pretreatment markedly preserved the resting platelet morphology and inhibited collagen-induced activation and shape changes. Further, the granule secretion, integrin-αIIbβ3 signaling, and the MAPK and PI3K/Akt pathways were also concentration-dependently inhibited. The in vivo blood flow rate and mice survival were improved, and H&E staining further revealed a concentration-dependent prevention of arterial occlusion following X. strumarium treatment. Conclusions: Collectively, X. strumarium demonstrated potent antiplatelet and antithrombotic effects, improving blood flow and survival while preventing arterial occlusion. Full article
(This article belongs to the Special Issue Platelets in Human Health and Diseases)
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15 pages, 2133 KB  
Article
Simulated Microgravity Causes Delayed Platelet Activation and Downregulates Acid-Sensing Ion Channel 1/2 Protein Expression
by Niharika Bala, Ling Yu, Neil S. Harris, Faisal Mukhtar and Abdel A. Alli
Biomedicines 2025, 13(12), 2860; https://doi.org/10.3390/biomedicines13122860 - 24 Nov 2025
Viewed by 331
Abstract
Background: Microgravity is a physical force that affects cellular functions, including gene expression, cellular differentiation, proliferation, and signal transduction. Ion channels play an important role in ionic permeability and cell physiology. In addition, ion channels have been shown to contribute to volume regulation, [...] Read more.
Background: Microgravity is a physical force that affects cellular functions, including gene expression, cellular differentiation, proliferation, and signal transduction. Ion channels play an important role in ionic permeability and cell physiology. In addition, ion channels have been shown to contribute to volume regulation, fluid homeostasis, blood pressure regulation, mechanosensation, and cell migration. The lipid composition and fluidity of the plasma membrane of various cell types contribute to the regulation of ion channels. We hypothesized that protein expression of acid-sensing ion channels (ASICs) is decreased while membrane fluidity is increased, leading to delayed activation of human platelets subject to microgravity conditions. Methods and Results: Platelets were maintained in simulated microgravity conditions using the rotating wall vessel method. Thromboelastography analysis showed there is a delay in platelet activation in human platelet samples subject to simulated microgravity conditions compared to normal gravity for 5 days at 37 °C. Western blotting and immunofluorescence microscopy studies showed that ASIC1/2 proteins are significantly downregulated in human platelets subject to the same simulated microgravity conditions. In addition, membrane fluidity was increased while sphingomyelin concentration was decreased in human platelets subject to simulated microgravity compared to normal gravity conditions. Conclusions: Taken together, the data from this study suggest that simulated microgravity delays platelet activation in human platelets in a mechanism presumably involving a decrease in ASIC1/2 protein expression and sphingomyelin plasma membrane concentration. Full article
(This article belongs to the Special Issue Platelets in Human Health and Diseases)
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