Role of Oxidative Stress in the Pathogenesis of Thrombotic Diseases

A special issue of Antioxidants (ISSN 2076-3921). This special issue belongs to the section "Health Outcomes of Antioxidants and Oxidative Stress".

Deadline for manuscript submissions: closed (30 April 2022) | Viewed by 4252

Special Issue Editors


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Guest Editor
Department of Pharmaceutical and Pharmacological Sciences, University of Padua, 35131 Padua, Italy
Interests: structure and function of protein coagulation factors; thrombin allostery; role of oxidative stress in the structure and function of the von willebrand factor; role of oxidative stress in the immunogenicity of plant food protein allergens; non-canonical activation of blood coagulation; structure and function of β2-glycoprotein-1 in health and disease; study of protein structure and dynamics by HDX-MS

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Guest Editor
Department of Translational Medicine and Surgery, Catholic University of the Sacred Heart, Rome, Italy
Interests: structure and function of the von Willebrand factor; role of oxidative stress on coagulation proteins in diabetes; structure, function and natural mutations of ADAMTS13; allosteric regulation of thrombin; pharmacokinetics of FVIII; venous thrombotic complications in cirrhosis; pharmacokinetics and pharmacodynamics of direct oral anticoagulants

Special Issue Information

Dear Colleagues

Thrombotic diseases are the leading cause of mortality worldwide. Endothelial dysfunction appears in the early stages of the pathogenesis of thrombotic disorders at both the arterial and venous circulatory compartments. The vascular endothelial surface normally creates, in fact, a non-thrombogenic structure. When an endothelial injury occurs in association with factors such as increased oxidative stress (OS) and cytokine storm, this may lead to deranged coagulation and platelet activation. Thus, OS, related to an imbalance between the production of oxygen free radicals and the antioxidant defense system, (superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GSH-Px), has been strongly implicated in thrombotic diseases.  

Many studies have shown that increased oxygen-free radicals, responsible for both lipid and protein oxidation, are involved in the pathogenesis of endothelial dysfunction, thrombosis, and organ damage. OS is also a relevant mediator of abnormal platelet function, as well as dysfunctional endothelium-dependent vasodilatation in cardiovascular disorders.

We invite you to submit your latest research findings or a review article to this Special Issue, which will bring together current research concerning the linkage between OS and thrombotic diseases. We welcome submissions concerning both basic research and clinical studies. We believe that this Special Issue on “Role of Oxidative Stress in the Pathogenesis of Thrombotic Diseases” will help to highlight the most recent advances on all aspects of this topic.

We look forward to your expert contribution, we send our kindest regards. 

Prof. Dr. Vincenzo De Filippis
Prof. Dr. Raimondo De Cristofaro
Guest Editors

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Keywords

  • Oxidative stress of lipids and proteins in cardiovascular diseases
  • Oxidative stress effects on coagulation proteins/enzymes
  • Antioxidants mechanisms in physiology and cardiovascular diseases
  • Methods to assess oxidative stress in thrombotic disorders
  • Oxidative stress and blood platelet function

Published Papers (1 paper)

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38 pages, 2080 KiB  
Review
Role of Oxidative Stress in the Pathogenesis of Atherothrombotic Diseases
by Giovanna Petrucci, Alessandro Rizzi, Duaa Hatem, Giulia Tosti, Bianca Rocca and Dario Pitocco
Antioxidants 2022, 11(7), 1408; https://0-doi-org.brum.beds.ac.uk/10.3390/antiox11071408 - 20 Jul 2022
Cited by 22 | Viewed by 3787
Abstract
Oxidative stress is generated by the imbalance between reactive oxygen species (ROS) formation and antioxidant scavenger system’s activity. Increased ROS, such as superoxide anion, hydrogen peroxide, hydroxyl radical and peroxynitrite, likely contribute to the development and complications of atherosclerotic cardiovascular diseases (ASCVD). In [...] Read more.
Oxidative stress is generated by the imbalance between reactive oxygen species (ROS) formation and antioxidant scavenger system’s activity. Increased ROS, such as superoxide anion, hydrogen peroxide, hydroxyl radical and peroxynitrite, likely contribute to the development and complications of atherosclerotic cardiovascular diseases (ASCVD). In genetically modified mouse models of atherosclerosis, the overexpression of ROS-generating enzymes and uncontrolled ROS formation appear to be associated with accelerated atherosclerosis. Conversely, the overexpression of ROS scavenger systems reduces or stabilizes atherosclerotic lesions, depending on the genetic background of the mouse model. In humans, higher levels of circulating biomarkers derived from the oxidation of lipids (8-epi-prostaglandin F, and malondialdehyde), as well as proteins (oxidized low-density lipoprotein, nitrotyrosine, protein carbonyls, advanced glycation end-products), are increased in conditions of high cardiovascular risk or overt ASCVD, and some oxidation biomarkers have been reported as independent predictors of ASCVD in large observational cohorts. In animal models, antioxidant supplementation with melatonin, resveratrol, Vitamin E, stevioside, acacetin and n-polyunsaturated fatty acids reduced ROS and attenuated atherosclerotic lesions. However, in humans, evidence from large, placebo-controlled, randomized trials or prospective studies failed to show any athero-protective effect of antioxidant supplementation with different compounds in different CV settings. However, the chronic consumption of diets known to be rich in antioxidant compounds (e.g., Mediterranean and high-fish diet), has shown to reduce ASCVD over decades. Future studies are needed to fill the gap between the data and targets derived from studies in animals and their pathogenetic and therapeutic significance in human ASCVD. Full article
(This article belongs to the Special Issue Role of Oxidative Stress in the Pathogenesis of Thrombotic Diseases)
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