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Antioxidants
Special Issues
Redox-Dependent Regulation of Haemostasis in Health and Disease
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Redox-Dependent Regulation of Haemostasis in Health and Disease

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 (31 August 2021) | Viewed by 13914

Special Issue Editor

Dr. Giordano Pula

E-Mail Website
Guest Editor
Universitätsklinikum Hamburg-Eppendorf und Medizinische Fakultät, Hamburg, Germany

Special Issue Information

Dear Colleagues,

Haemostasis is the homeostatic response of the human body to injury and bleeding. Haemostasis is typically divided into primary haemostasis, in which circulating platelets play a pivotal role, and secondary haemostasis, consisting of the activation of the coagulation cascade leading to fibrin deposition and ultimately blood clotting. The distinction between primary and secondary haemostasis is only conceptual. In reality, these two responses are tightly entwined, with platelets promoting coagulation and coagulation activating platelets via thrombin. Canonical post-translational protein modifications regulate both platelets and coagulation, with protein phosphorylation central to platelet function and proteolytic activation of native zymogens pivotal for coagulation. In addition, a growing body of evidence suggests that oxidative post-translational modification of plasma proteins, blood cells and vascular tissues is involved in normal primary and secondary haemostasis in physiological conditions. Interestingly, oxidative stress leads to the dysregulation of protein oxidation in the circulatory system, which participates in the development of the thrombotic complications associated with human vascular diseases. In this collection, we aim to present our current understanding of how oxidant molecules and the enzyme responsible for their generation control the human vascular system both in health and disease.

Dr. Giordano Pula
Guest Editor

Manuscript Submission Information

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Keywords

  • haemostasis
  • platelet
  • coagulation
  • endothelial
  • thrombosis
  • oxidative stress
  • oxidant
  • redox

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Published Papers (3 papers)

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Research

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16 pages, 2514 KiB  
Article
Protein Disulphide Isomerase and NADPH Oxidase 1 Cooperate to Control Platelet Function and Are Associated with Cardiometabolic Disease Risk Factors
by Renato Simões Gaspar, Tanya Sage, Gemma Little, Neline Kriek, Giordano Pula and Jonathan M. Gibbins
Antioxidants 2021, 10(3), 497; https://doi.org/10.3390/antiox10030497 - 23 Mar 2021
Cited by 12 | Viewed by 3726
Abstract
Background: Protein disulphide isomerase (PDI) and NADPH oxidase 1 (Nox-1) regulate platelet function and reactive oxygen species (ROS) generation, suggesting potentially interdependent roles. Increased platelet reactivity and ROS production have been correlated with cardiometabolic disease risk factors. Objectives: To establish whether PDI and [...] Read more.
Background: Protein disulphide isomerase (PDI) and NADPH oxidase 1 (Nox-1) regulate platelet function and reactive oxygen species (ROS) generation, suggesting potentially interdependent roles. Increased platelet reactivity and ROS production have been correlated with cardiometabolic disease risk factors. Objectives: To establish whether PDI and Nox-1 cooperate to control platelet function. Methods: Immunofluorescence microscopy was utilised to determine expression and localisation of PDI and Nox-1. Platelet aggregation, fibrinogen binding, P-selectin exposure, spreading and calcium mobilization were measured as markers of platelet function. A cross-sectional population study (n = 136) was conducted to assess the relationship between platelet PDI and Nox-1 levels and cardiometabolic risk factors. Results: PDI and Nox-1 co-localized upon activation induced by the collagen receptor GPVI. Co-inhibition of PDI and Nox-1 led to additive inhibition of GPVI-mediated platelet aggregation, activation and calcium flux. This was confirmed in murine Nox-1−/− platelets treated with PDI inhibitor bepristat, without affecting bleeding. PDI and Nox-1 together contributed to GPVI signalling that involved the phosphorylation of p38 MAPK, p47phox, PKC and Akt. Platelet PDI and Nox-1 levels were upregulated in obesity, with platelet Nox-1 also elevated in hypertensive individuals. Conclusions: We show that PDI and Nox-1 cooperate to control platelet function and are associated with cardiometabolic risk factors. Full article
(This article belongs to the Special Issue Redox-Dependent Regulation of Haemostasis in Health and Disease)
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Review

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20 pages, 1579 KiB  
Review
Clotting Dysfunction in Sepsis: A Role for ROS and Potential for Therapeutic Intervention
by Maria Elisa Lopes-Pires, Jéssica Oliveira Frade-Guanaes and Gregory J. Quinlan
Antioxidants 2022, 11(1), 88; https://doi.org/10.3390/antiox11010088 - 30 Dec 2021
Cited by 30 | Viewed by 5092
Abstract
Sepsis is regarded as one of the main causes of death among the critically ill. Pathogen infection results in a host-mediated pro-inflammatory response to fight infection; as part of this response, significant endogenous reactive oxygen (ROS) and nitrogen species (RNS) production occurs, instigated [...] Read more.
Sepsis is regarded as one of the main causes of death among the critically ill. Pathogen infection results in a host-mediated pro-inflammatory response to fight infection; as part of this response, significant endogenous reactive oxygen (ROS) and nitrogen species (RNS) production occurs, instigated by a variety of sources, including activated inflammatory cells, such as neutrophils, platelets, and cells from the vascular endothelium. Inflammation can become an inappropriate self-sustaining and expansive process, resulting in sepsis. Patients with sepsis often exhibit loss of aspects of normal vascular homeostatic control, resulting in abnormal coagulation events and the development of disseminated intravascular coagulation. Diagnosis and treatment of sepsis remain a significant challenge for healthcare providers globally. Targeting the drivers of excessive oxidative/nitrosative stress using antioxidant treatments might be a therapeutic option. This review focuses on the association between excessive oxidative/nitrosative stress, a common feature in sepsis, and loss of homeostatic control at the level of the vasculature. The literature relating to potential antioxidants is also described. Full article
(This article belongs to the Special Issue Redox-Dependent Regulation of Haemostasis in Health and Disease)
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Other

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12 pages, 1081 KiB  
Perspective
Diabetes and Thrombosis: A Central Role for Vascular Oxidative Stress
by Aishwarya R. Vaidya, Nina Wolska, Dina Vara, Reiner K. Mailer, Katrin Schröder and Giordano Pula
Antioxidants 2021, 10(5), 706; https://doi.org/10.3390/antiox10050706 - 29 Apr 2021
Cited by 20 | Viewed by 4337
Abstract
Diabetes mellitus is the fifth most common cause of death worldwide. Due to its chronic nature, diabetes is a debilitating disease for the patient and a relevant cost for the national health system. Type 2 diabetes mellitus is the most common form of [...] Read more.
Diabetes mellitus is the fifth most common cause of death worldwide. Due to its chronic nature, diabetes is a debilitating disease for the patient and a relevant cost for the national health system. Type 2 diabetes mellitus is the most common form of diabetes mellitus (90% of cases) and is characteristically multifactorial, with both genetic and environmental causes. Diabetes patients display a significant increase in the risk of developing cardiovascular disease compared to the rest of the population. This is associated with increased blood clotting, which results in circulatory complications and vascular damage. Platelets are circulating cells within the vascular system that contribute to hemostasis. Their increased tendency to activate and form thrombi has been observed in diabetes mellitus patients (i.e., platelet hyperactivity). The oxidative damage of platelets and the function of pro-oxidant enzymes such as the NADPH oxidases appear central to diabetes-dependent platelet hyperactivity. In addition to platelet hyperactivity, endothelial cell damage and alterations of the coagulation response also participate in the vascular damage associated with diabetes. Here, we present an updated interpretation of the molecular mechanisms underlying vascular damage in diabetes, including current therapeutic options for its control. Full article
(This article belongs to the Special Issue Redox-Dependent Regulation of Haemostasis in Health and Disease)
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