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Molecular and Cellular Advances in Coagulation and Bleeding
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Molecular and Cellular Advances in Coagulation and Bleeding

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

Deadline for manuscript submissions: 10 September 2026 | Viewed by 330

Special Issue Editor

Dr. Muriel Meiring

E-Mail Website
Guest Editor
1. Department of Haematology and Cell Biology, School of Pathology, Faculty of Health Sciences, University of the Free State, Bloemfontein, South Africa
2. Department of Haematology and Cell Biology, Universitas Academic Laboratories, National Health Laboratory Service, Bloemfontein, South Africa
Interests: immunity; antibodies; leukemia; thombotic and haemostatic disorders

Special Issue Information

Dear Colleagues,

This Special Issue focuses on emerging molecular trends in thrombotic and haemostatic disorders, highlighting cutting-edge research and innovative therapeutic strategies. It encompasses manuscripts that explore the intricate interplay between inflammation and coagulation, emphasizing the cross-talk that drives pathological clot formation. Topics include novel approaches to anticoagulation targeting the contact activation or tissue factor pathway, as well as advances in platelet signalling and metabolic reprogramming that influence thrombotic risk. The issue also addresses post-translational modifications of coagulation proteins, which play a critical role in regulating the haemostatic balance. Furthermore, it covers proteomics and molecular biomarkers for improved diagnosis and prognosis, alongside RNA-based therapeutics and gene-editing technologies that promise precision medicine solutions. Finally, the role of extracellular vesicles in coagulation and thrombosis is examined, offering insights into their potential as diagnostic tools and therapeutic targets. Collectively, these contributions aim to advance the understanding and treatment of thrombotic disorders and haemostatic disorders at the molecular level.

Dr. Muriel Meiring
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 250 words) can be sent to the Editorial Office for assessment.

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

  • thrombosis
  • haemostasis
  • inflammation-coagulation cross ralk
  • proteomics
  • molecular biomarkers

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Published Papers (1 paper)

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Research

16 pages, 2281 KB  
Article
Allosteric and ATP-Pocket BCR::ABL1 Inhibition In Vitro, and Characterising Ex Vivo Thrombo-Inflammatory Biomarkers and Thrombin Generation in Asciminib-Treated CML Patients
by Musab M. A. Omar, Majed A. Alanazi, David T. Yeung, Timothy P. Hughes and Denise E. Jackson
Int. J. Mol. Sci. 2026, 27(8), 3623; https://doi.org/10.3390/ijms27083623 - 18 Apr 2026
Viewed by 146
Abstract
Chronic myeloid leukaemia (CML) is driven by the t(9;22) forming the BCR::ABL1 fusion gene, leading to the development of hyper-myeloid proliferation. This led to development of tyrosine kinase inhibitors (TKIs) such as Imatinib, Nilotinib, and Ponatinib. However, resistance or intolerance to ATP-competitive TKIs [...] Read more.
Chronic myeloid leukaemia (CML) is driven by the t(9;22) forming the BCR::ABL1 fusion gene, leading to the development of hyper-myeloid proliferation. This led to development of tyrosine kinase inhibitors (TKIs) such as Imatinib, Nilotinib, and Ponatinib. However, resistance or intolerance to ATP-competitive TKIs remains a challenge for some patients. asciminib (ABL001), a novel TKI, targets the myristoyl pocket of ABL1 instead of the ATP-binding site, reducing resistance to mutations. As asciminib is linked to thrombocytopenia, its effects on platelet activation, endothelial function, and inflammation must be studied to assess its potential to promote thrombosis. The main objective of this study is to determine the potential of asciminib as a monotherapy in inducing pathological responses to platelets and endothelium over time within the vasculature. This study assessed the effects of TKIs including asciminib on platelets and thrombotic biomarkers. Washed platelets were used to measure granule secretion, thrombus formation, surface expression of glycoproteins, apoptosis, and viability. Plasma from chronically Asciminib-treated CML patients was analysed using sandwich ELISA for inflammatory and platelet–endothelial biomarkers, and thrombin generation assays were performed to study coagulation. This approach combined in vitro and ex vivo methods to explore the impact of asciminib on platelet function and thrombotic potential. The study shows that acute treatment with asciminib does not promote platelet activation or thrombus formation. Instead, it exhibits an inhibitory effect on thrombus formation in vitro and is associated with reduced thrombo-inflammatory biomarkers ex vivo in chronically treated CML patients. Asciminib was associated with increased thrombin generation over time, suggesting an effect on secondary haemostasis. Asciminib does not appear to induce a prothrombotic or proinflammatory state under the conditions studied, which may be advantageous for CML patients. However, the observed increase in thrombin generation over time suggests a potential effect on secondary haemostasis that warrants further investigation in controlled studies. Full article
(This article belongs to the Special Issue Molecular and Cellular Advances in Coagulation and Bleeding)
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