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New Advances in Thrombosis 2.0
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New Advances in Thrombosis 2.0

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: closed (30 January 2024) | Viewed by 5204

Special Issue Editor

Dr. Isabella Russo

E-Mail Website
Guest Editor
Department of Clinical and Biological Sciences, University of Turin, Regione Gonzole, 10, Orbassano, I-10043 Turin, Italy
Interests: platelets function; nitric oxide; haemostasis; thrombosis; anti-platelet drugs; platelet dysfunction in metabolic diseases
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Thrombosis occurs when a thrombus forms inside blood vessels, thus disrupting blood flow. It represents a major complication of cardio- and cerebrovascular events, such as myocardial infarction, acute ischemic stroke, or venous thromboembolism.

The components of thrombi include fibrin, red blood cells, platelets, leukocytes, and neutrophil extracellular traps, and this heterogeneous composition is deeply influenced by the specific location in which it develops and by the disease etiopathogenesis.

Furthermore, there is increasing interest in extracellular vesicles that are released by many cells through membrane shedding and that can contribute to transferring biological messages far from the triggering event, as well as be used as biomarkers of thrombo-embolic pathology.

Considering the high prevalence of the thrombotic scenarios associated with metabolic and atherosclerotic diseases, the aim of the current Special Issue is to share the latest scientific achievements in the field of biological and molecular mechanisms involved in impaired coagulation, platelet reactivity, and/or fibrinolysis.

Focus on studies should be related to:

  • Explanation of thrombosis pathogenetic mechanisms;
  • Searching for new biomarkers for the detection of prothrombotic risk;
  • The use of new research techniques on thrombus study.

Both original and review articles providing new insights into the subject are invited.

Dr. Isabella Russo
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.

Keywords

  • thrombosis
  • platelets
  • coagulation
  • diabetes
  • obesity
  • insulin resistance
  • metabolic disease
  • cardiovascular diseases

Published Papers (6 papers)

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Research

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18 pages, 4447 KiB  
Article
Characterization of Biomarkers of Thrombo-Inflammation in Patients with First-Diagnosed Atrial Fibrillation
by Julian Friebel, Max Wegner, Leon Blöbaum, Philipp-Alexander Schencke, Kai Jakobs, Marianna Puccini, Emily Ghanbari, Stella Lammel, Tharusan Thevathasan, Verena Moos, Marco Witkowski, Ulf Landmesser and Ursula Rauch-Kröhnert
Int. J. Mol. Sci. 2024, 25(7), 4109; https://doi.org/10.3390/ijms25074109 - 08 Apr 2024
Viewed by 461
Abstract
Patients with first-diagnosed atrial fibrillation (FDAF) exhibit major adverse cardiovascular events (MACEs) during follow-up. Preclinical models have demonstrated that thrombo-inflammation mediates adverse cardiac remodeling and atherothrombotic events. We have hypothesized that thrombin activity (FIIa) links coagulation with inflammation and cardiac fibrosis/dysfunction. Surrogate markers [...] Read more.
Patients with first-diagnosed atrial fibrillation (FDAF) exhibit major adverse cardiovascular events (MACEs) during follow-up. Preclinical models have demonstrated that thrombo-inflammation mediates adverse cardiac remodeling and atherothrombotic events. We have hypothesized that thrombin activity (FIIa) links coagulation with inflammation and cardiac fibrosis/dysfunction. Surrogate markers of the thrombo-inflammatory response in plasma have not been characterized in FDAF. In this prospective longitudinal study, patients presenting with FDAF (n = 80), and 20 matched controls, were included. FIIa generation and activity in plasma were increased in the patients with early AF compared to the patients with chronic cardiovascular disease without AF (controls; p < 0.0001). This increase was accompanied by elevated biomarkers (ELISA) of platelet and endothelial activation in plasma. Pro-inflammatory peripheral immune cells (TNF-α+ or IL-6+) that expressed FIIa-activated protease-activated receptor 1 (PAR1) (flow cytometry) circulated more frequently in patients with FDAF compared to the controls (p < 0.0001). FIIa activity correlated with cardiac fibrosis (collagen turnover) and cardiac dysfunction (NT-pro ANP/NT-pro BNP) surrogate markers. FIIa activity in plasma was higher in patients with FDAF who experienced MACE. Signaling via FIIa might be a presumed link between the coagulation system (tissue factor-FXa/FIIa-PAR1 axis), inflammation, and pro-fibrotic pathways (thrombo-inflammation) in FDAF. Full article
(This article belongs to the Special Issue New Advances in Thrombosis 2.0)
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12 pages, 1288 KiB  
Article
Thrombelastography and Conventional Coagulation Markers in Chronic Obstructive Pulmonary Disease: A Prospective Paired-Measurements Study Comparing Exacerbation and Stable Phases
by Ema Rastoder, Peter Kamstrup, Caroline Hedsund, Alexander Jordan, Pradeesh Sivapalan, Valdemar Rømer, Frederikke Falkvist, Sadaf Hamidi, Elisabeth Bendstrup, Søren Sperling, Maria Dons, Tor Biering-Sørensen, Casper Falster, Christian B. Laursen, Jørn Carlsen and Jens-Ulrik Stæhr Jensen
Int. J. Mol. Sci. 2024, 25(4), 2051; https://doi.org/10.3390/ijms25042051 - 08 Feb 2024
Viewed by 669
Abstract
Chronic Obstructive Pulmonary Disease (COPD) exacerbation is known for its substantial impact on morbidity and mortality among affected patients, creating a significant healthcare burden worldwide. Coagulation abnormalities have emerged as potential contributors to exacerbation pathogenesis, raising concerns about increased thrombotic events during exacerbation. [...] Read more.
Chronic Obstructive Pulmonary Disease (COPD) exacerbation is known for its substantial impact on morbidity and mortality among affected patients, creating a significant healthcare burden worldwide. Coagulation abnormalities have emerged as potential contributors to exacerbation pathogenesis, raising concerns about increased thrombotic events during exacerbation. The aim of this study was to explore the differences in thrombelastography (TEG) parameters and coagulation markers in COPD patients during admission with exacerbation and at a follow-up after discharge. This was a multi-center cohort study. COPD patients were enrolled within 72 h of hospitalization. The baseline assessments were Kaolin-TEG and blood samples. Statistical analysis involved using descriptive statistics; the main analysis was a paired t-test comparing coagulation parameters between exacerbation and follow-up. One hundred patients participated, 66% of whom were female, with a median age of 78.5 years and comorbidities including atrial fibrillation (18%) and essential arterial hypertension (45%), and sixty-five individuals completed a follow-up after discharge. No significant variations were observed in Kaolin-TEG or conventional coagulation markers between exacerbation and follow-up. The Activated Partial Thromboplastin Clotting Time (APTT) results were near-significant, with p = 0.08. In conclusion, TEG parameters displayed no significant alterations between exacerbation and follow-up. Full article
(This article belongs to the Special Issue New Advances in Thrombosis 2.0)
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Review

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16 pages, 2660 KiB  
Review
A Comprehensive Retrospective Study on the Mechanisms of Cyclic Mechanical Stretch-Induced Vascular Smooth Muscle Cell Death Underlying Aortic Dissection and Potential Therapeutics for Preventing Acute Aortic Aneurysm and Associated Ruptures
by Jing Zhao and Masanori Yoshizumi
Int. J. Mol. Sci. 2024, 25(5), 2544; https://doi.org/10.3390/ijms25052544 - 22 Feb 2024
Viewed by 527
Abstract
Acute aortic dissection (AAD) and associated ruptures are the leading causes of death in cardiovascular diseases (CVDs). Hypertension is a prime risk factor for AAD. However, the molecular mechanisms underlying AAD remain poorly understood. We previously reported that cyclic mechanical stretch (CMS) leads [...] Read more.
Acute aortic dissection (AAD) and associated ruptures are the leading causes of death in cardiovascular diseases (CVDs). Hypertension is a prime risk factor for AAD. However, the molecular mechanisms underlying AAD remain poorly understood. We previously reported that cyclic mechanical stretch (CMS) leads to the death of rat aortic smooth muscle cells (RASMCs). This review focuses on the mechanisms of CMS-induced vascular smooth muscle cell (VSMC) death. Moreover, we have also discussed the potential therapeutics for preventing AAD and aneurysm ruptures. Full article
(This article belongs to the Special Issue New Advances in Thrombosis 2.0)
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28 pages, 1307 KiB  
Review
Factors Influencing Venous Remodeling in the Development of Varicose Veins of the Lower Limbs
by Lukasz Gwozdzinski, Anna Pieniazek and Krzysztof Gwozdzinski
Int. J. Mol. Sci. 2024, 25(3), 1560; https://doi.org/10.3390/ijms25031560 - 26 Jan 2024
Cited by 1 | Viewed by 1390
Abstract
One of the early symptoms of chronic venous disease (CVD) is varicose veins (VV) of the lower limbs. There are many etiological environmental factors influencing the development of chronic venous insufficiency (CVI), although genetic factors and family history of the disease play a [...] Read more.
One of the early symptoms of chronic venous disease (CVD) is varicose veins (VV) of the lower limbs. There are many etiological environmental factors influencing the development of chronic venous insufficiency (CVI), although genetic factors and family history of the disease play a key role. All these factors induce changes in the hemodynamic in the venous system of the lower limbs leading to blood stasis, hypoxia, inflammation, oxidative stress, proteolytic activity of matrix metalloproteinases (MMPs), changes in microcirculation and, consequently, the remodeling of the venous wall. The aim of this review is to present current knowledge on CVD, including the pathophysiology and mechanisms related to vein wall remodeling. Particular emphasis has been placed on describing the role of inflammation and oxidative stress and the involvement of extracellular hemoglobin as pathogenetic factors of VV. Additionally, active substances used in the treatment of VV were discussed. Full article
(This article belongs to the Special Issue New Advances in Thrombosis 2.0)
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Graphical abstract

24 pages, 2121 KiB  
Review
To Gain Insights into the Pathophysiological Mechanisms of the Thrombo-Inflammatory Process in the Atherosclerotic Plaque
by Francesco Nappi
Int. J. Mol. Sci. 2024, 25(1), 47; https://doi.org/10.3390/ijms25010047 - 19 Dec 2023
Viewed by 1077
Abstract
Thromboinflammation, the interplay between thrombosis and inflammation, is a significant pathway that drives cardiovascular and autoimmune diseases, as well as COVID-19. SARS-CoV-2 causes inflammation and blood clotting issues. Innate immune cells have emerged as key modulators of this process. Neutrophils, the most predominant [...] Read more.
Thromboinflammation, the interplay between thrombosis and inflammation, is a significant pathway that drives cardiovascular and autoimmune diseases, as well as COVID-19. SARS-CoV-2 causes inflammation and blood clotting issues. Innate immune cells have emerged as key modulators of this process. Neutrophils, the most predominant white blood cells in humans, are strategically positioned to promote thromboinflammation. By releasing decondensed chromatin structures called neutrophil extracellular traps (NETs), neutrophils can initiate an organised cell death pathway. These structures are adorned with histones, cytoplasmic and granular proteins, and have cytotoxic, immunogenic, and prothrombotic effects that can hasten disease progression. Protein arginine deiminase 4 (PAD4) catalyses the citrullination of histones and is involved in the release of extracellular DNA (NETosis). The neutrophil inflammasome is also required for this process. Understanding the link between the immunological function of neutrophils and the procoagulant and proinflammatory activities of monocytes and platelets is important in understanding thromboinflammation. This text discusses how vascular blockages occur in thromboinflammation due to the interaction between neutrophil extracellular traps and ultra-large VWF (von Willebrand Factor). The activity of PAD4 is important for understanding the processes that drive thromboinflammation by linking the immunological function of neutrophils with the procoagulant and proinflammatory activities of monocytes and platelets. This article reviews how vaso-occlusive events in thrombo-inflammation occur through the interaction of neutrophil extracellular traps with von Willebrand factor. It highlights the relevance of PAD4 in neutrophil inflammasome assembly and neutrophil extracellular traps in thrombo-inflammatory diseases such as atherosclerosis and cardiovascular disease. Interaction between platelets, VWF, NETs and inflammasomes is critical for the progression of thromboinflammation in several diseases and was recently shown to be active in COVID-19. Full article
(This article belongs to the Special Issue New Advances in Thrombosis 2.0)
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Other

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10 pages, 1322 KiB  
Case Report
Aberrant Platelet Aggregation as Initial Presentation of Essential Thrombocythemia: Failure of Entero-Coated Aspirin to Reduce Platelet Hyperactivation
by Alessandro Morotti, Cristina Barale, Michele Sornatale, Emilia Giugliano, Vittorio Emanuele Muccio, Chiara Frascaroli, Marisa Pautasso, Alessandro Fornari and Isabella Russo
Int. J. Mol. Sci. 2024, 25(1), 176; https://doi.org/10.3390/ijms25010176 - 22 Dec 2023
Viewed by 636
Abstract
Essential thrombocythemia (ET) is a myeloproliferative neoplasm variant characterized by excessive production of platelets. Since the most common cause of mortality and morbidity in ET patients is thrombosis, the excessive production of platelets may cause thrombotic events. However, little is known about the [...] Read more.
Essential thrombocythemia (ET) is a myeloproliferative neoplasm variant characterized by excessive production of platelets. Since the most common cause of mortality and morbidity in ET patients is thrombosis, the excessive production of platelets may cause thrombotic events. However, little is known about the function of platelets in ET. We report a female patient who presented as asymptomatic, without a remarkable medical history, and ET was diagnosed after an incidental finding of moderate thrombocytosis. Notably, together with thrombocytosis, an abnormal platelet phenotype was found for the presence of a massive, rapid and spontaneous formation of aggregates and platelet hypersensitivity to subthreshold concentrations of aggregating agonists. Bone marrow histopathological examination and genetic analysis with the JAK2 (V617F) gene mutation findings confirmed the initial suspicion of ET. Although the ET patient was placed on aspirin, the persistence of the platelet hyperactivation and hyperaggregability prompted a switch in antiplatelet medication from entero-coated (EC) to plain aspirin. As result, platelet hypersensitivity to agonists and spontaneous aggregation were no longer found. Collectively, our study demonstrates that platelet function analysis could be a reliable predictor of ET and that plain aspirin should be preferred over EC aspirin to attenuate platelet hyperreactivity. Full article
(This article belongs to the Special Issue New Advances in Thrombosis 2.0)
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