Vascular Disease and Thrombosis

A special issue of Biomolecules (ISSN 2218-273X). This special issue belongs to the section "Molecular Medicine".

Deadline for manuscript submissions: closed (30 June 2024) | Viewed by 2773

Special Issue Editor

Special Issue Information

Dear Colleagues,

We are seeking submissions for a Special Issue of Biomolecules on vascular disease and thrombosis.

Vascular disease and thrombosis cause morbidity and mortality worldwide. In this area, on the venous side, the most common clinical manifestation is a venous thromboembolism (VTE) (this includes superficial and deep vein thrombosis, pulmonary embolism, and post-thrombotic syndrome). On the arterial side, the most common clinical manifestations are ischemic heart disease (including acute myocardial infarction), ischemic stroke, acute limb ischemia, intestinal infarction, etc. Research focused on biomolecular events is crucial to the prevention and treatment of thrombovascular diseases.

For this Special Issue, both research and review articles (general and systematic) are welcome.

Dr. Raffaele Serra
Guest Editor

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Keywords

  • venous thromboembolism
  • superficial vein thrombosis
  • deep vein thrombosis
  • pulmonary embolism
  • post-thrombotic syndrome
  • ischemic heart disease
  • acute myocardial infarction
  • ischemic stroke
  • acute limb ischemia
  • intestinal infarction
  • biomarkers
  • hematologic disorders
  • thrombophilias

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Published Papers (2 papers)

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Research

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15 pages, 4090 KiB  
Article
Identification of Genes and miRNAs Associated with TAFI-Related Thrombosis: An in Silico Study
by Erasmia Rouka, Sotirios G. Zarogiannis, Chrissi Hatzoglou, Konstantinos I. Gourgoulianis and Foteini Malli
Biomolecules 2023, 13(9), 1318; https://doi.org/10.3390/biom13091318 - 28 Aug 2023
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Abstract
Thrombin-Activatable Fibrinolysis Inhibitor (TAFI) is a carboxypeptidase B-like proenzyme encoded by the CPB2 gene. After thrombin activation, TAFI downregulates fibrinolysis, thus linking the latter with coagulation. TAFI has been shown to play a role in venous and arterial thrombotic diseases, yet, data regarding [...] Read more.
Thrombin-Activatable Fibrinolysis Inhibitor (TAFI) is a carboxypeptidase B-like proenzyme encoded by the CPB2 gene. After thrombin activation, TAFI downregulates fibrinolysis, thus linking the latter with coagulation. TAFI has been shown to play a role in venous and arterial thrombotic diseases, yet, data regarding the molecular mechanisms underlying its function have been conflicting. In this study, we focused on the prediction and functional enrichment analysis (FEA) of the TAFI interaction network and the microRNAs (miRNAs) targeting the members of this network in an attempt to identify novel components and pathways of TAFI-related thrombosis. To this end, we used nine bioinformatics software tools. We found that the TAFI interactome consists of 28 unique genes mainly involved in hemostasis. Twenty-four miRNAs were predicted to target these genes. Co-annotation analysis of the predicted interactors with respect to Kyoto Encyclopedia of Genes and Genomes (KEGG) pathways and transcription factors (TFs) pointed to the complement and coagulation cascades as well as neutrophil extracellular trap formation. Cancer, stroke, and intracranial aneurysm were among the top 20 significant diseases related to the identified miRNAs. We reason that the predicted biomolecules should be further studied in the context of TAFI-related thrombosis. Full article
(This article belongs to the Special Issue Vascular Disease and Thrombosis)
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Review

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16 pages, 1055 KiB  
Review
Molecular Insight into Acute Limb Ischemia
by Davide Costa, Nicola Ielapi, Paolo Perri, Roberto Minici, Teresa Faga, Ashour Michael, Umberto Marcello Bracale, Michele Andreucci and Raffaele Serra
Biomolecules 2024, 14(7), 838; https://doi.org/10.3390/biom14070838 - 11 Jul 2024
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Abstract
Acute limb ischemia (ALI) is defined as a sudden reduction in blood flow to a limb, resulting in cessation of blood flow and, therefore, cessation of the delivery of nutrients and oxygen to the tissues of the lower limb. Despite optimal treatment to [...] Read more.
Acute limb ischemia (ALI) is defined as a sudden reduction in blood flow to a limb, resulting in cessation of blood flow and, therefore, cessation of the delivery of nutrients and oxygen to the tissues of the lower limb. Despite optimal treatment to restore blood flow to ischemic tissues, some patients may suffer from ischemia/reperfusion (I/R) syndrome, the most severe complication after a revascularization procedure used to restore blood flow. There are multiple molecular and cellular factors that are involved in each phase of ALI. This review focuses firstly on molecular and cellular factors of arterial thrombosis, highlighting the role of atherosclerotic plaques, smooth muscle cells (SMCs), and cytokine which may alter key components of the extracellular matrix (ECM). Then, molecular and cellular factors of arterial embolism will be discussed, highlighting the importance of thrombi composition. Molecular and cellular factors of ischemia/reperfusion syndrome are analyzed in depth, highlighting several important mechanisms related to tissue damage, such as inflammation, apoptosis, autophagy, necrosis, and necroptosis. Furthermore, local and general complications of ALI are discussed in the context of molecular alterations. Ultimately, the role of novel biomarkers and targeted therapies is discussed. Full article
(This article belongs to the Special Issue Vascular Disease and Thrombosis)
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