Search for Articles:
Title / Keyword
Author / Affiliation / Email
Journal
Article Type
 
 
Advanced Search
 
Section
Special Issue
Volume
Issue
Number
Page
 
5.2
3.9
Journals
Biomedicines
Special Issues
Molecular Researches in Pro-thrombotic Disorders
share announcement

Molecular Researches in Pro-thrombotic Disorders

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

Deadline for manuscript submissions: closed (31 March 2024) | Viewed by 16648

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

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

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

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 polices can be found here.

Published Papers (7 papers)

Download All Papers
Order results
Result details
Show export options expand_more Show export options expand_less
Select all
Export citation of selected articles as:

Research

Jump to: Review

12 pages, 689 KiB  
Article
Dysregulated Coagulation and Fibrinolysis Are Present in Patients Admitted to the Emergency Department with Acute Hypoxemic Respiratory Failure: A Prospective Study
by Chrysi Keskinidou, Alice Georgia Vassiliou, Elena Papoutsi, Edison Jahaj, Ioanna Dimopoulou, Ilias Siempos and Anastasia Kotanidou
Biomedicines 2024, 12(5), 1081; https://doi.org/10.3390/biomedicines12051081 - 13 May 2024
Viewed by 1055
Abstract
Acute hypoxemic respiratory failure (AHRF) is defined as acute and progressive, and patients are at a greater risk of developing acute respiratory distress syndrome (ARDS). Until now, most studies have focused on prognostic and diagnostic biomarkers in ARDS. Since there is evidence supporting [...] Read more.
Acute hypoxemic respiratory failure (AHRF) is defined as acute and progressive, and patients are at a greater risk of developing acute respiratory distress syndrome (ARDS). Until now, most studies have focused on prognostic and diagnostic biomarkers in ARDS. Since there is evidence supporting a connection between dysregulated coagulant and fibrinolytic pathways in ARDS progression, it is plausible that this dysregulation also exists in AHRF. The aim of this study was to explore whether levels of soluble endothelial protein C receptor (sEPCR) and plasminogen differentiate patients admitted to the emergency department (ED) with AHRF. sEPCR and plasminogen levels were measured in 130 AHRF patients upon ED presentation by ELISA. Our results demonstrated that patients presenting to the ED with AHRF had elevated levels of sEPCR and plasminogen. It seems that dysregulation of coagulation and fibrinolysis occur in the early stages of respiratory failure requiring hospitalisation. Further research is needed to fully comprehend the contribution of sEPCR and plasminogen in AHRF. Full article
(This article belongs to the Special Issue Molecular Researches in Pro-thrombotic Disorders)
►▼ Show Figures

Figure 1

11 pages, 3050 KiB  
Article
Platelet Adhesion Mediated by von Willebrand Factor at High Shear Rates Is Associated with Premature Coronary Artery Disease
by Sergey Okhota, Sergey Kozlov, Yuliya Avtaeva, Ivan Melnikov, Olga Saburova, Konstantin Guria, Evgeny Matroze and Zufar Gabbasov
Biomedicines 2023, 11(7), 1916; https://doi.org/10.3390/biomedicines11071916 - 6 Jul 2023
Cited by 1 | Viewed by 1163
Abstract
This study investigated von Willebrand factor (VWF)-mediated platelet adhesion at high shear rates in patients with premature coronary artery disease (CAD). The study included 84 patients with stable premature CAD and 64 patients without CAD. Whole blood samples were perfused through a microfluidic [...] Read more.
This study investigated von Willebrand factor (VWF)-mediated platelet adhesion at high shear rates in patients with premature coronary artery disease (CAD). The study included 84 patients with stable premature CAD and 64 patients without CAD. Whole blood samples were perfused through a microfluidic cell over a collagen-coated surface at a shear rate of 1300 s−1. Measurements were performed before and after the inhibition of VWF-specific platelet GPIb receptors with an anti-GPIb monoclonal antibody (mAb). Platelet adhesion decreased by 77.0% (55.9; 84.7) in patients with premature CAD and by 29.6% (0.0; 59.7) in control patients after the inhibition of VWF–platelet interaction with anti-GPIb mAb (p < 0.001). After adjusting for traditional risk factors, the odds ratio for premature CAD per 1% decrease in GPIb-mediated platelet adhesion was 1.03 (95% CI, 1.02–1.05; p < 0.001). The optimal cut-off level value of GPIb-mediated platelet adhesion was 62.8%, with 70.2% sensitivity and 81.2% specificity for CAD. The plasma levels of VWF or antiplatelet therapy did not affect the GPIb-mediated component of platelet adhesion. Thus, the GPIb-mediated component of platelet adhesion was more pronounced in patients with premature CAD. This may indicate the possible role of excessive VWF–platelet interactions in the development of premature CAD. Full article
(This article belongs to the Special Issue Molecular Researches in Pro-thrombotic Disorders)
►▼ Show Figures

Figure 1

12 pages, 2297 KiB  
Article
Hemostasis System and Plasminogen Activity in Retrochorial Hematoma in the First Trimester of Pregnancy
by Natalia B. Tikhonova, Natalya B. Kuznetsova, Andrey P. Milovanov, Eugene I. Goufman, Tatiana V. Fokina, Andrey P. Aleksankin, Valentina V. Aleksankina, Irina I. Stepanova, Alexandr A. Stepanov, Marina N. Boltovskaya and Natalia V. Nizyaeva
Biomedicines 2022, 10(9), 2284; https://doi.org/10.3390/biomedicines10092284 - 14 Sep 2022
Cited by 1 | Viewed by 1925
Abstract
(1) Background: The components of the fibrinolytic system and its main component, plasminogen, play a key role in the first months of pregnancy. The effect of autoantibodies interacting with plasminogen in the formation of retrochorial hematoma is unknown. The aim of our study [...] Read more.
(1) Background: The components of the fibrinolytic system and its main component, plasminogen, play a key role in the first months of pregnancy. The effect of autoantibodies interacting with plasminogen in the formation of retrochorial hematoma is unknown. The aim of our study was to determine the role of plasminogen and IgA, IgM, and IgG, which bind to plasminogen, in retrochorial hematoma. (2) Methods: Prothrombin time (PT), thrombin time (TT), partial activated thromboplastin time (aPTT), soluble fibrin-monomer complex (SFMC), D-dimer, plasminogen activity (%Plg), plasminogen concentration (Plg), and the levels of IgG (IgG-Plg), IgM (IgM-Plg), IgA (IgA-Plg) interacting with plasminogen were determined in plasma samples of 57 women with normal pregnancy and 16 with retrochorial hematoma. (3) Results: %Plg in plasma samples from women with retrochorial hematoma was significantly lower than in plasma samples from women with normal pregnancy. The diagnostic significance of %Plg in the ROC analysis was AUC = 0.85. A direct correlation was found between aPTT and the level of autologous IgM interacting with plasminogen. (4) Conclusions: A decrease in the activity of plasminogen in the blood serum of women in the first trimester of pregnancy may indicate disturbances in the hemostasis system and the formation of retrochorial hematoma. According to the results of the study, it is possible to recommend the determination of plasminogen activity in the management of pregnant women in gynecological practice. Full article
(This article belongs to the Special Issue Molecular Researches in Pro-thrombotic Disorders)
►▼ Show Figures

Figure 1

11 pages, 996 KiB  
Article
Circulating Microvesicles in Association with the NLRP3 Inflammasome in Coronary Thrombi from STEMI Patients
by Vibeke Bratseth, Jostein Nordeng, Ragnhild Helseth, Svein Solheim, Sissel Åkra, Harald Arnesen, Gemma Chiva-Blanch and Ingebjørg Seljeflot
Biomedicines 2022, 10(9), 2196; https://doi.org/10.3390/biomedicines10092196 - 5 Sep 2022
Viewed by 1998
Abstract
Microvesicles (MVs) are actively secreted by cells. The NLRP3-inflammasome and the interleukin 6 (IL-6)-pathways are central in cardiovascular disease. Knowledge of how the inflammasome influences the MVs is limited. In a cross-sectional study, we assessed whether MVs in plasma associate with genes encoding [...] Read more.
Microvesicles (MVs) are actively secreted by cells. The NLRP3-inflammasome and the interleukin 6 (IL-6)-pathways are central in cardiovascular disease. Knowledge of how the inflammasome influences the MVs is limited. In a cross-sectional study, we assessed whether MVs in plasma associate with genes encoding inflammasome signalling in coronary thrombi. Moreover, any relationships between inflammasome activation and phosphatidylserine (PS) externalization, determined through Annexin V (AV+) labelling, and myocardial injury, assessed by cardiac troponin T (cTnT), were analysed. Intracoronary thrombi and blood samples from STEMI patients (n = 33) were investigated. mRNA of NLRP3, caspase-1, interleukin-1β (IL-1β), interleukin-18 (IL-18), IL-6, soluble IL-6-receptor (sIL-6R), and glycoprotein-130 (gp130) were isolated from the thrombi and relatively quantified by RT-PCR. MVs were analysed by flow cytometry. Total AV+ MVs, mainly reflecting hypercoagulability, correlated positively to NLRP3 gene expression (r = 0.545, p = 0.009). A similar pattern was seen for platelet, endothelial and leukocyte derived MVs, separately. The majority of the MVs were AV− (96%). Total and AV− MVs correlated inversely with IL-1β (r = −0.399 and −0.438, respectively, p < 0.05, both) and gp130 (r = −0.457 and −0.502, respectively, p < 0.05, both). No correlations between MVs and cTnT were observed. Our findings indicate an association between NLRP3-inflammasome in coronary thrombi and procoagulant AV+ MVs in STEMI patients. The inverse relationships between AV− MVs and the gene expression of inflammasome activation may indicate an immuno-dampening role of this subpopulation. Full article
(This article belongs to the Special Issue Molecular Researches in Pro-thrombotic Disorders)
►▼ Show Figures

Figure 1

19 pages, 4224 KiB  
Article
Angiopoietin-2 Inhibition of Thrombomodulin-Mediated Anticoagulation—A Novel Mechanism That May Contribute to Hypercoagulation in Critically Ill COVID-19 Patients
by Michael Hultström, Karin Fromell, Anders Larsson, Barbro Persson, Bo Nilsson, Susan E. Quaggin, Christer Betsholtz, Robert Frithiof, Miklos Lipcsey and Marie Jeansson
Biomedicines 2022, 10(6), 1333; https://doi.org/10.3390/biomedicines10061333 - 6 Jun 2022
Cited by 13 | Viewed by 3316
Abstract
Hypercoagulation and endothelial dysfunction play central roles in severe forms of COVID-19 infections, but the molecular mechanisms involved are unclear. Increased plasma levels of the inflammatory cytokine and TIE2 receptor antagonist Angiopoietin-2 were reported in severely ill COVID-19 patients. In vitro experiments suggest [...] Read more.
Hypercoagulation and endothelial dysfunction play central roles in severe forms of COVID-19 infections, but the molecular mechanisms involved are unclear. Increased plasma levels of the inflammatory cytokine and TIE2 receptor antagonist Angiopoietin-2 were reported in severely ill COVID-19 patients. In vitro experiments suggest that Angiopoietin-2 bind and inhibits thrombomodulin. Thrombomodulin is expressed on the luminal surface of endothelial cells where it is an important member of the intrinsic anticoagulant pathway through activation of protein C. Using clinical data, mouse models, and in vitro assays, we tested if Angiopoietin-2 plays a causal role in COVID-19-associated hypercoagulation through direct inhibition of thrombin/thrombomodulin-mediated physiological anticoagulation. Angiopoietin-2 was measured in 61 patients at admission, and after 10 days in the 40 patients remaining in the ICU. We found that Angiopoietin-2 levels were increased in COVID-19 patients in correlation with disease severity, hypercoagulation, and mortality. In support of a direct effect of Angiopoietin-2 on coagulation, we found that injected Angiopoietin-2 in mice associated to thrombomodulin and resulted in a shortened tail bleeding time, decreased circulating levels of activated protein C, and increased plasma thrombin/antithrombin complexes. Conversely, bleeding time was increased in endothelial-specific Angiopoietin-2 knockout mice, while knockout of Tie2 had no effect on tail bleeding. Using in vitro assays, we found that Angiopoietin-2 inhibited thrombomodulin-mediated anticoagulation and protein C activation in human donor plasma. Our data suggest a novel in vivo mechanism for Angiopoietin-2 in COVID-19-associated hypercoagulation, implicating that Angiopoietin-2 inhibitors may be effective in the treatment of hypercoagulation in severe COVID-19 infection. Full article
(This article belongs to the Special Issue Molecular Researches in Pro-thrombotic Disorders)
►▼ Show Figures

Figure 1

Review

Jump to: Research

35 pages, 5286 KiB  
Review
Fibrinaloid Microclots and Atrial Fibrillation
by Douglas B. Kell, Gregory Y. H. Lip and Etheresia Pretorius
Biomedicines 2024, 12(4), 891; https://doi.org/10.3390/biomedicines12040891 - 17 Apr 2024
Cited by 2 | Viewed by 2531
Abstract
Atrial fibrillation (AF) is a comorbidity of a variety of other chronic, inflammatory diseases for which fibrinaloid microclots are a known accompaniment (and in some cases, a cause, with a mechanistic basis). Clots are, of course, a well-known consequence of atrial fibrillation. We [...] Read more.
Atrial fibrillation (AF) is a comorbidity of a variety of other chronic, inflammatory diseases for which fibrinaloid microclots are a known accompaniment (and in some cases, a cause, with a mechanistic basis). Clots are, of course, a well-known consequence of atrial fibrillation. We here ask the question whether the fibrinaloid microclots seen in plasma or serum may in fact also be a cause of (or contributor to) the development of AF. We consider known ‘risk factors’ for AF, and in particular, exogenous stimuli such as infection and air pollution by particulates, both of which are known to cause AF. The external accompaniments of both bacterial (lipopolysaccharide and lipoteichoic acids) and viral (SARS-CoV-2 spike protein) infections are known to stimulate fibrinaloid microclots when added in vitro, and fibrinaloid microclots, as with other amyloid proteins, can be cytotoxic, both by inducing hypoxia/reperfusion and by other means. Strokes and thromboembolisms are also common consequences of AF. Consequently, taking a systems approach, we review the considerable evidence in detail, which leads us to suggest that it is likely that microclots may well have an aetiological role in the development of AF. This has significant mechanistic and therapeutic implications. Full article
(This article belongs to the Special Issue Molecular Researches in Pro-thrombotic Disorders)
►▼ Show Figures

Figure 1

23 pages, 2692 KiB  
Review
Association between COVID-19 Diagnosis and Coronary Artery Thrombosis: A Narrative Review
by Francesco Nappi, Omar Giacinto, Omar Ellouze, Antonio Nenna, Sanjeet Singh Avtaar Singh, Massimo Chello, Assine Bouzguenda and Xavier Copie
Biomedicines 2022, 10(3), 702; https://doi.org/10.3390/biomedicines10030702 - 18 Mar 2022
Cited by 15 | Viewed by 3538
Abstract
Coronavirus disease 2019 is characterized by its severe respiratory effects. Data early on indicated an increased risk of mortality in patients with cardiovascular comorbidities. Early reports highlighted the multisystem inflammatory syndrome, cytokine storm, and thromboembolic events as part of the disease processes. The [...] Read more.
Coronavirus disease 2019 is characterized by its severe respiratory effects. Data early on indicated an increased risk of mortality in patients with cardiovascular comorbidities. Early reports highlighted the multisystem inflammatory syndrome, cytokine storm, and thromboembolic events as part of the disease processes. The aim of this review is to assess the association between COVID-19 and its thrombotic complications, specifically related to the cardiovascular system. The role of neutrophil extracellular traps (NETs) is explored in the pathogenesis of the disease. The structure and anatomy of the virus are pivotal to its virulence in comparison to other α and β Coronaviridae (HCoV-229E, HCoV-OC43, HCoV-229E, HCoV-NL63, HCoV-OC43, and HCoV-HKU1). In particular, the host interaction and response may explain the variability of severity in patients. Angio tensin-converting enzyme 2 (ACE2) activation may be implicated in the cardiovascular and throm bogenic potential of the disease. The virus may also have direct effects on the endothelial lining affecting hemostasis and resulting in thrombosis through several mechanisms. Dipyridamole may have a therapeutic benefit in NET suppression. Therapeutic avenues should be concentrated on the different pathophysiological steps involving the virus and the host. Full article
(This article belongs to the Special Issue Molecular Researches in Pro-thrombotic Disorders)
►▼ Show Figures

Figure 1

Show export options expand_more Show export options expand_less
Select all
Export citation of selected articles as:
 
Displaying articles 1-7
Back to TopTop