Submit to Special Issue Submit Abstract to Special Issue Review for IJMS Propose a Special Issue

Journal Menu

Journal Browser

Molecular Insights into Thrombosis

Special Issue Editors
Special Issue Information
Benefits of Publishing in a Special Issue
Published Papers

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Pathology, Diagnostics, and Therapeutics".

Deadline for manuscript submissions: 30 August 2025 | Viewed by 13949

Share This Special Issue

Special Issue Editor

Prof. Dr. J. Kh. Khizroeva

E-Mail Website
Guest Editor

Department of Obstetrics, Gynecology and Perinatal Medicine, I.M. Sechenov First Moscow State Medical University of the Ministry of Health of the Russian Federation (Sechenov University), Moscow 119992, Russia
Interests: thrombosis

Special Issue Information

Dear Colleagues,

In the practice of a doctor of any specialty, blood clotting disorders, thrombosis, thromboembolism, hemorrhagic diathesis and massive bleeding occupy a special place, since they pose the highest risk of disability and fatal complications. The management of patients of this profile in all countries of the world is one of the most responsible tasks of a doctor. It requires knowledge of modern achievements of biology and medicine, especially pathology and physiology of hemostasis - an interdisciplinary science, without which the development of modern clinical medicine is unthinkable today. The most important key to understanding the pathogenesis of thrombohemorrhagic complications is the knowledge of systemic syndromes: disseminated intravascular coagulation syndrome, antiphospholipid syndrome, systemic inflammatory response syndrome, thrombotic microangiopathy which form multifaceted relationships in the absolute majority of diseases. Moreover, thrombosis is a major health problem that affects morbidity and mortality of cancer patients. Knowledge of pathogenesis and correct diagnosis is primarily the basis for effective prevention of thromboembolic complications and require the involvement of knowledge from various fields of medicine.

Prof. Dr. J. Kh. Khizroeva
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.

Benefits of Publishing in a Special Issue

Ease of navigation: Grouping papers by topic helps scholars navigate broad scope journals more efficiently.
Greater discoverability: Special Issues support the reach and impact of scientific research. Articles in Special Issues are more discoverable and cited more frequently.
Expansion of research network: Special Issues facilitate connections among authors, fostering scientific collaborations.
External promotion: Articles in Special Issues are often promoted through the journal's social media, increasing their visibility.
e-Book format: Special Issues with more than 10 articles can be published as dedicated e-books, ensuring wide and rapid dissemination.

Further information on MDPI's Special Issue policies can be found here.

Published Papers (6 papers)

Download All Papers

Order results

Result details

Show export options Show export options

Select all

Export citation of selected articles as:

Research

Jump to: Review

12 pages, 2777 KiB

Open AccessArticle

Inhibition of Cancer Cell Migration and Invasion In Vitro by Recombinant Tyrosine-Sulfated Haemathrin, A Thrombin Inhibitor

by Guk Heui Jo, Sun Ah Jung, Jin Sook Yoon and Joon H. Lee

Int. J. Mol. Sci. 2024, 25(21), 11822; https://doi.org/10.3390/ijms252111822 - 4 Nov 2024

Viewed by 1163

Abstract

Thrombin, a key enzyme in the regulation of hemostasis, has been implicated in cancer progression. This study explored the effect of recombinant tyrosine-sulfated haemathrin on cancer cell behavior and signaling pathways compared to wild-type (WT) haemathrin 2. The recombinant proteins, tyrosine-sulfated haemathrin 2 (haemathrin 2S), and WT haemathrin 2 were produced in Escherichia coli and subsequently purified and applied to SKOV3 and MDA-MB-231 cells with and without thrombin stimulation. Cell migration and invasion were assessed using wound healing and Transwell assays, respectively. Haemathrin 2S treatment significantly diminished cell migration and invasion promoted by thrombin in both SKOV3 and MDA-MB-231 cells (p < 0.05). Additionally, haemathrin 2S effectively inhibited thrombin-induced phosphorylation of serine/threonine kinase (Akt) in both cell lines (p < 0.05), while WT haemathrin 2 had this effect only in MDA-MB-231 cells. Furthermore, haemathrin 2S significantly reduced thrombin-activated phosphorylation of extracellular signal-regulated kinases (ERK) and p38 in both cell lines (p < 0.05) and reversed E/N-cadherin expression in thrombin-treated MDA-MB-231 cells (p < 0.05), which were not observed with WT haemathrin 2. Overall, haemathrin 2S was more effective than WT haemathrin 2 in reducing cancer cell migration and invasion, indicating that targeting thrombin with sulfated haemathrin is a promising strategy for cancer therapy. However, further in vivo studies are needed to confirm these results. Full article

(This article belongs to the Special Issue Molecular Insights into Thrombosis)

► Show Figures

Figure 1

20 pages, 1896 KiB

Open AccessArticle

Analysis of the Model of Atherosclerosis Formation in Pig Hearts as a Result of Impaired Activity of DNA Repair Enzymes

by Robert Paslawski, Paweł Kowalczyk, Urszula Paslawska, Jerzy Wiśniewski, Piotr Dzięgiel, Adrian Janiszewski, Liliana Kiczak, Maciej Zacharski, Barbara Gawdzik, Karol Kramkowski and Andrzej Szuba

Int. J. Mol. Sci. 2024, 25(4), 2282; https://doi.org/10.3390/ijms25042282 - 14 Feb 2024

Cited by 3 | Viewed by 2033

Abstract

Excessive consumption of food rich in saturated fatty acids and carbohydrates can lead to metabolic disturbances and cardiovascular disease. Hyperlipidemia is a significant risk factor for acute cardiac events due to its association with oxidative stress. This leads to arterial wall remodeling, including an increase in the thickness of the intima media complex (IMT), and endothelial dysfunction leading to plaque formation. The decreased nitric oxide synthesis and accumulation of lipids in the wall result in a reduction in the vasodilating potential of the vessel. This study aimed to establish a clear relationship between markers of endothelial dysfunction and the activity of repair enzymes in cardiac tissue from a pig model of early atherosclerosis. The study was conducted on 28 female Polish Landrace pigs, weighing 40 kg (approximately 3.5 months old), which were divided into three groups. The control group (n = 11) was fed a standard, commercial, balanced diet (BDG) for 12 months. The second group (n = 9) was fed an unbalanced, high-calorie Western-type diet (UDG). The third group (n = 8) was fed a Western-type diet for nine months and then switched to a standard, balanced diet (regression group, RG). Control examinations, including blood and urine sampling, were conducted every three months under identical conditions with food restriction for 12 h and water restriction for four hours before general anesthesia. The study analyzed markers of oxidative stress formed during lipid peroxidation processes, including etheno DNA adducts, ADMA, and NEFA. These markers play a crucial role in reactive oxygen species analysis in ischemia–reperfusion and atherosclerosis in mammalian tissue. Essential genes involved in oxidative-stress-induced DNA demethylation like OGG1 (8-oxoguanine DNA glycosylase), MPG (N-Methylpurine DNA Glycosylase), TDG (Thymine-DNA glycosylase), APEX (apurinic/apirymidinic endodeoxyribonuclease 1), PTGS2 (prostaglandin-endoperoxide synthase 2), and ALOX (Arachidonate Lipoxygenase) were measured using the Real-Time RT-PCR method. The data suggest that high oxidative stress, as indicated by TBARS levels, is associated with high levels of DNA repair enzymes and depends on the expression of genes involved in the repair pathway. In all analyzed groups of heart tissue homogenates, the highest enzyme activity and gene expression values were observed for the OGG1 protein recognizing the modified 8oxoG. Conclusion: With the long-term use of an unbalanced diet, the levels of all DNA repair genes are increased, especially (significantly) Apex, Alox, and Ptgs, which strongly supports the hypothesis that an unbalanced diet induces oxidative stress that deregulates DNA repair mechanisms and may contribute to genome instability and tissue damage. Full article

(This article belongs to the Special Issue Molecular Insights into Thrombosis)

► Show Figures

Graphical abstract

11 pages, 954 KiB

Open AccessArticle

Factor XI in Carriers of Antiphospholipid Antibodies: Elevated Levels Associated with Symptomatic Thrombotic Cases, While Low Levels Linked to Asymptomatic Cases

by Javier Pagán-Escribano, Javier Corral, Antonia Miñano, José Padilla, Vanessa Roldán, María Julia Hernández-Vidal, Jesús Lozano, Isabel de la Morena-Barrio, Vicente Vicente, María Luisa Lozano, María Teresa Herranz and María Eugenia de la Morena-Barrio

Int. J. Mol. Sci. 2023, 24(22), 16270; https://doi.org/10.3390/ijms242216270 - 13 Nov 2023

Cited by 1 | Viewed by 1431

Abstract

Antiphospholipid syndrome (APS) is a thromboinflammatory disorder caused by circulating antiphospholipid autoantibodies (aPL) and characterized by an increased risk of thrombotic events. The pathogenic mechanisms of these antibodies are complex and not fully understood, but disturbances in coagulation and fibrinolysis have been proposed to contribute to the thrombophilic state. This study aims to evaluate the role of an emerging hemostatic molecule, FXI, in the thrombotic risk of patients with aPL. Cross-sectional and observational study of 194 consecutive and unrelated cases with aPL recruited in a single center: 82 asymptomatic (AaPL) and 112 with primary antiphospholipid syndrome (APS). Clinical and epidemiological variables were collected. The profile of aPL was determined. Plasma FXI was evaluated by Western blotting and two coagulation assays (FXI:C). In cases with low FXI, molecular analysis of the F11 gene was performed. FXI:C levels were significantly higher in patients with APS than in patients with AaPL (122.8 ± 33.4 vs. 104.5 ± 27.5; p < 0.001). Multivariate analysis showed a significant association between symptomatic patients with aPL (APS) and high FXI (>150%) (OR = 11.57; 95% CI: 1.47–90.96; p = 0.020). In contrast, low FXI (<70%), mostly caused by inhibitors, was less frequent in the group of patients with APS compared to AaPL (OR = 0.17; 95%CI: 0.36–0.86; p = 0.032). This study suggests that FXI levels may play a causal role in the prothrombotic state induced by aPLs and holds the promise of complementary treatments in APS patients by targeting FXI. Full article

(This article belongs to the Special Issue Molecular Insights into Thrombosis)

► Show Figures

Figure 1

Review

Jump to: Research

26 pages, 735 KiB

Open AccessReview

Combining Colchicine and Antiplatelet Therapy to Tackle Atherothrombosis: A Paradigm in Transition?

by Salvatore Giordano, Marina Camera, Marta Brambilla, Gianmarco Sarto, Luigi Spadafora, Marco Bernardi, Antonio Iaconelli, Domenico D’Amario, Giuseppe Biondi-Zoccai, Alessandra Ida Celia, Elena Tremoli, Giacomo Frati, Dominick J. Angiolillo, Sebastiano Sciarretta and Mattia Galli

Int. J. Mol. Sci. 2025, 26(3), 1136; https://doi.org/10.3390/ijms26031136 - 28 Jan 2025

Cited by 2 | Viewed by 1658

Abstract

Atherothrombosis, the primary driver of acute cardiovascular (CV) events, is characterized by the activation of three key pathophysiological pathways: platelets, coagulation, and inflammation. Dual antiplatelet therapy (DAPT) is the current standard of care for patients with acute coronary syndrome, providing significant reductions in cardiovascular (CV) events, albeit with an associated increased risk of bleeding. However, the high residual risk of recurrent events among these patients highlights the need for alternative strategies to treat and prevent atherothrombosis. To this extent, several approaches aimed at targeting atherothrombosis have been proposed. Among these, a strategy of dual-pathway inhibition simultaneously targeting platelets, using single or DAPT, and coagulation, using a low-dose anticoagulant such as rivaroxaban 2.5 mg twice daily, has shown to reduce CV events but at the expense of increased bleeding. Targeting inflammatory pathways has the potential to be a highly effective strategy to tackle atherothrombosis without increasing bleeding risk. Several anti-inflammatory agents have been tested in patients with coronary artery disease, but to date only colchicine is approved for secondary prevention on top of standard care, including antiplatelet therapy. However, many aspects of colchicine’s mechanism of action, including its antiplatelet effects and how it synergizes with antiplatelet therapy, remain unclear. In this review, we summarize the available clinical and pre-clinical evidence on the antiplatelet effects of colchicine and its synergistic interactions with antiplatelet therapy, highlighting their potential role in addressing atherothrombosis. Full article

(This article belongs to the Special Issue Molecular Insights into Thrombosis)

► Show Figures

Figure 1

26 pages, 1673 KiB

Open AccessReview

Research into New Molecular Mechanisms in Thrombotic Diseases Paves the Way for Innovative Therapeutic Approaches

by Sara Sacchetti, Chiara Puricelli, Marco Mennuni, Valentina Zanotti, Luca Giacomini, Mara Giordano, Umberto Dianzani, Giuseppe Patti and Roberta Rolla

Int. J. Mol. Sci. 2024, 25(5), 2523; https://doi.org/10.3390/ijms25052523 - 21 Feb 2024

Cited by 4 | Viewed by 2779

Abstract

Thrombosis is a multifaceted process involving various molecular components, including the coagulation cascade, platelet activation, platelet–endothelial interaction, anticoagulant signaling pathways, inflammatory mediators, genetic factors and the involvement of various cells such as endothelial cells, platelets and leukocytes. A comprehensive understanding of the molecular signaling pathways and cell interactions that play a role in thrombosis is essential for the development of precise therapeutic strategies for the treatment and prevention of thrombotic diseases. Ongoing research in this field is constantly uncovering new molecular players and pathways that offer opportunities for more precise interventions in the clinical setting. These molecular insights into thrombosis form the basis for the development of targeted therapeutic approaches for the treatment and prevention of thrombotic disease. The aim of this review is to provide an overview of the pathogenesis of thrombosis and to explore new therapeutic options. Full article

(This article belongs to the Special Issue Molecular Insights into Thrombosis)

► Show Figures

Figure 1

16 pages, 583 KiB

Open AccessReview

The Hemostatic System in Newborns and the Risk of Neonatal Thrombosis

by Jamilya Khizroeva, Alexander Makatsariya, Alexander Vorobev, Victoria Bitsadze, Ismail Elalamy, Arina Lazarchuk, Polina Salnikova, Sabina Einullaeva, Antonina Solopova, Maria Tretykova, Alexandra Antonova, Tamara Mashkova, Kristina Grigoreva, Margaret Kvaratskheliia, Fidan Yakubova, Natalia Degtyareva, Valentina Tsibizova, Nilufar Gashimova and David Blbulyan

Int. J. Mol. Sci. 2023, 24(18), 13864; https://doi.org/10.3390/ijms241813864 - 8 Sep 2023

Cited by 14 | Viewed by 3715

Abstract

Newborns are the most vulnerable patients for thrombosis development among all children, with critically ill and premature infants being in the highest risk group. The upward trend in the rate of neonatal thrombosis could be attributed to progress in the treatment of severe neonatal conditions and the increased survival in premature babies. There are physiological differences in the hemostatic system between neonates and adults. Neonates differ in concentrations and rate of synthesis of most coagulation factors, turnover rates, the ability to regulate thrombin and plasmin, and in greater variability compared to adults. Natural inhibitors of coagulation (protein C, protein S, antithrombin, heparin cofactor II) and vitamin K-dependent coagulation factors (factors II, VII, IX, X) are low, but factor VIII and von Willebrand factor are elevated. Newborns have decreased fibrinolytic activity. In the healthy neonate, the balance is maintained but appears more easily converted into thrombosis. Neonatal hemostasis has less buffer capacity, and almost 95% of thrombosis is provoked. Different triggering risk factors are responsible for thrombosis in neonates, but the most important risk factors for thrombosis are central catheters, fluid fluctuations, liver dysfunction, and septic and inflammatory conditions. Low-molecular-weight heparins are the agents of choice for anticoagulation. Full article

(This article belongs to the Special Issue Molecular Insights into Thrombosis)

► Show Figures

Journal Menu

Journal Browser

Molecular Insights into Thrombosis

Share This Special Issue

Special Issue Editor

Special Issue Information

Benefits of Publishing in a Special Issue

Published Papers (6 papers)

Research

Review

Further Information

Guidelines

MDPI Initiatives

Follow MDPI