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Biomedicines
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Molecular Researches in Pro-Thrombotic Disorders—2nd Edition
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Molecular Researches in Pro-Thrombotic Disorders—2nd Edition

A special issue of Biomedicines (ISSN 2227-9059). This special issue belongs to the section "Molecular and Translational Medicine".

Deadline for manuscript submissions: closed (30 June 2025) | Viewed by 639

Special Issue Editor

Dr. Cristina Barale

E-Mail Website
Guest Editor
Department of Clinical and Biological Sciences, University of Turin, Turin, Italy
Interests: platelets; atherosclerosis; cardiovascular diseases; thrombosis; metabolic syndrome; diabetes; hypercholesterolemia; vascular smooth muscle cells; coagulation
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Cardiovascular and cerebrovascular diseases, chronic obstructive pulmonary disease, diabetes, and cancer are the leading causes of death worldwide. They share common ground in the form of inflammation that contributes to the onset of a systemic hypercoagulable state, initiating continuous crosstalk between phlogistic and thrombotic processes. In this context, vascular cells such as platelets, endothelial cells, pericytes, and inflammatory cells (i.e., neutrophils, macrophages), interact through a plethora of substances, including cytokines and chemokines that promote a prothrombotic state. The heterogeneous clinical sequelae include myocardial infarction, stroke, venous deep thrombosis and pulmonary embolisms, splanchnic thrombosis, and peripheral arterial disease. These complications worsen the prognosis and increase the mortality of any chronic disease.

This Special Issue welcomes original articles and reviews that contribute to understanding the molecular pathways involved in prothrombotic states; better comprehension of the molecular signaling that underlies such conditions could lead to the identification of new therapeutic mechanisms targets.

Dr. Cristina Barale
Guest Editor

Manuscript Submission Information

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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

  • inflammation
  • thrombosis
  • hypercoagulable state
  • coagulation cascade factors
  • chronic diseases
  • platelets
  • platelet activation
  • endothelial cells
  • neutrophils
  • macrophages

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Published Papers (1 paper)

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Research

19 pages, 5798 KiB  
Article
High-Dose Tranexamic Acid Enhances Circulating Neutrophil Extracellular Traps and Thrombus in Thrombosis Mouse Model
by Jung-Wook Song, Eun-Hye Seo, Un Yung Choi, Chung-Sik Oh, Aram Kim, Keeho Song, Seung-Hyun Lee and Jin Kook Kim
Biomedicines 2025, 13(6), 1284; https://doi.org/10.3390/biomedicines13061284 - 23 May 2025
Viewed by 531
Abstract
Background/Objectives: Tranexamic acid (TXA) reduces mortality in patients with massive hemorrhage by inhibiting fibrinolysis. However, it is associated with an increased risk of thrombosis. The activation of neutrophil extracellular traps (NETs) has been implicated in the formation of thrombosis. This study investigated [...] Read more.
Background/Objectives: Tranexamic acid (TXA) reduces mortality in patients with massive hemorrhage by inhibiting fibrinolysis. However, it is associated with an increased risk of thrombosis. The activation of neutrophil extracellular traps (NETs) has been implicated in the formation of thrombosis. This study investigated the effects of tranexamic acid on circulating and localized NETs, neutrophils, platelets, and the vascular endothelium in a mouse model of thrombosis. Methods: A ferric chloride-induced thrombosis mouse model was used and divided into five groups: a Control group that received intraperitoneal phosphate-buffered saline (PBS), and four experimental groups that received intraperitoneal tranexamic acid at doses of 5 mg/kg, 10 mg/kg, 20 mg/kg, and 30 mg/kg, respectively. To evaluate the expression of circulating and localized NETs, neutrophils, platelets, vascular endothelial cells, fibrinogen, and D-dimer, the following markers were analyzed: myeloperoxidase (MPO), neutrophil marker, cluster of differentiation (CD)31, CD34, fibrinogen α-chain, and D-dimer. These markers were assessed using flow cytometry, immunohistofluorescence staining, and Western blot analysis. The primary endpoint was the differential expression of anti-MPO antibody among the groups. Results: In total, data from 20 thrombosis mouse models were analyzed. For each group, four samples were assessed by flow cytometry, and three samples by immunohistofluorescence staining and Western blot analysis, respectively. In the flow cytometric analysis, circulating anti-MPO antibody expression was significantly higher in the TXA 20 and TXA 30 groups compared to the Control group (p = 0.001 and p = 0.001, respectively). Immunohistofluorescence staining revealed that D-dimer expression in the thrombotic femoral artery was significantly lower in the TXA 5, TXA 10, and TXA 20 groups compared to the Control group (p = 0.005; p = 0.018; p = 0.004, respectively), but significantly higher in the TXA 30 group than in the Control group (p = 0.044). Similarly, the expression of anti-fibrinogen antibody was significantly lower in the TXA 5, TXA 10, and TXA 20 groups compared to the Control group (p = 0.038; p = 0.003; p = 0.041, respectively). Western blot analysis showed no significant differences in the expression of anti-Ly6B.2, anti-fibrinogen, and anti-CD31 antibodies among the groups. Conclusions: The present study suggests that high-dose tranexamic acid (30 mg/kg) administration may increase circulating NETs and localized D-dimer levels, indicating a higher potential for thrombosis in a thrombosis mouse model. These findings imply that the prothrombotic effects of tranexamic acid may be dose-dependent and could vary based on underlying disease conditions. Therefore, the careful dosage adjustment of tranexamic acid may be necessary, particularly in patients at risk of thrombosis. Full article
(This article belongs to the Special Issue Molecular Researches in Pro-Thrombotic Disorders—2nd Edition)
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