Oxidative Stress and Inflammatory Mechanisms in Vascular Disorders

A special issue of Antioxidants (ISSN 2076-3921).

Deadline for manuscript submissions: closed (1 March 2023) | Viewed by 12385

Special Issue Editors

Institut de Recerca de l’Hospital de la Santa Creu i Sant Pau – Centre CERCA, Barcelona, Spain
Interests: inflammatory mechanisms involves in cardiovascular diseases; eicosanoids in the cardiovascular context; biomarkers for early diagnosis of cardiovascular diseases; mechanisms underlying the development of aortic abdominal aneurysm (AAA); correlation between biochemical and structural alterations of the aortic wall and the clinical parameters of patients with AAA; analysis of genes regulated by hypoxia/ischemia; neovascularization
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear colleagues,

Cardiovascular diseases are the leading cause of death worldwide and involve several pathologies such as disorders of the coronary and peripheral arteries as well as cerebrovascular diseases. In addition, chronic inflammatory disorders have been identified as cardiovascular risks, and recent research has revealed the contribution of various inflammatory cells to vascular oxidative stress.

Inflammation is one of the key intermediate pathways involved in developing cardiovascular disorders, including atherosclerotic plaque development and rupture, aortic aneurysm formation, angiogenesis, and ischemia/reperfusion damage. Inflammation is a protective response of an organism to injury to localize, eliminate, and remove harmful stimuli and recover damaged tissues. The inflammatory response becomes pathogenic when it occurs at an inappropriate site or is excessive in extent or duration. Reactive oxygen species (ROS) are involved in the initiation, progression, and resolution of the inflammatory response in vascular disease. The activation of immune cells and recruitment to vascular tissues by cardiovascular risk factors lead to the activation of vascular ROS sources, which contribute to vascular dysfunction and the progression of the disease. Oxidative stress is defined by an imbalance between the production of ROS and the capacity of the antioxidant system to counteract the deleterious effects of oxidants. At physiological concentrations, ROS act as important mediators involved in regulating cell proliferation and differentiation, cell adhesion, migration, wound healing, angiogenesis, etc. In contrast, overproduction of ROS may result in cell and tissue injury and contribute to the development and progression of the inflammatory state underlying vascular diseases.

We invite you to submit your latest research findings or a review article to this Special Issue, which will bring together current research concerning oxidative stress and inflammatory mechanisms in vascular disorders.

Dr. Mercedes Camacho Pérez de Madrid
Dr. Josep Julve
Guest Editors

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. Antioxidants 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 2900 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

  • Oxidative stress
  • Inflammation
  • Cardiovascular diseases
  • Antioxidant therapy
  • Antinflammatory drugs
  • Abdominal Aortic Aneurysm
  • Peripheral Arterial disease
  • Atherosclerosis

Published Papers (4 papers)

Order results
Result details
Select all
Export citation of selected articles as:

Research

Jump to: Review

21 pages, 2634 KiB  
Article
Contribution of Elevated Glucose and Oxidized LDL to Macrophage Inflammation: A Role for PRAS40/Akt-Dependent Shedding of Soluble CD14
by Lucía Sanjurjo, Esmeralda Castelblanco, Josep Julve, Nuria Villalmanzo, Érica Téllez, Anna Ramirez-Morros, Núria Alonso, Dídac Mauricio and Maria-Rosa Sarrias
Antioxidants 2023, 12(5), 1083; https://0-doi-org.brum.beds.ac.uk/10.3390/antiox12051083 - 11 May 2023
Viewed by 2179
Abstract
Atherosclerosis, a process in which macrophages play a key role, is accelerated in diabetes. Elevated concentrations of serum-oxidized low-density lipoproteins (oxLDL) represent a common feature of both conditions. The main goal of this study was to determine the contribution of oxLDL to the [...] Read more.
Atherosclerosis, a process in which macrophages play a key role, is accelerated in diabetes. Elevated concentrations of serum-oxidized low-density lipoproteins (oxLDL) represent a common feature of both conditions. The main goal of this study was to determine the contribution of oxLDL to the inflammatory response of macrophages exposed to diabetic-mimicking conditions. THP1 cells and peripheral blood monocytes purified from non-diabetic healthy donors were cultured under normal (5 mM) or high glucose (HG) (15 mM) with oxLDL. Then, foam cell formation, expression of CD80, HLADR, CD23, CD206, and CD163, as well as toll-like receptor 4 (TLR4) and co-receptors CD36 and CD14 (both at the cell surface and soluble (sCD14)), and inflammatory mediators’ production were measured by flow cytometry, RT-qPCR, or ELISA. Additionally, serum sCD14 was determined in subjects with subclinical atherosclerosis with and without diabetes by ELISA. Our results showed that oxLDL-mediated intracellular lipid accumulation via CD36 increased under HG and that HG + oxLDL enhanced TNF, IL1B, and IL8, and decreased IL10. Moreover, TLR4 was upregulated in macrophages under HG and monocytes of subjects with diabetes and atherosclerosis. Interestingly, HG-oxLDL upregulated CD14 gene expression, although its total cellular protein abundance remained unaltered. sCD14 shedding via PRAS40/Akt-dependent mechanisms, with pro-inflammatory activity, was significantly increased in cultured macrophages and plasma from subjects with diabetes and subclinical atherosclerosis or hypercholesterolemia. Our data support an enhanced synergistic pro-inflammatory effect induced by HG and oxLDL in cultured human macrophages, possibly explained by increased sCD14 shedding. Full article
(This article belongs to the Special Issue Oxidative Stress and Inflammatory Mechanisms in Vascular Disorders)
Show Figures

Graphical abstract

17 pages, 1834 KiB  
Article
Electronegative LDL Is Associated with Plaque Vulnerability in Patients with Ischemic Stroke and Carotid Atherosclerosis
by Núria Puig, Pol Camps-Renom, Arnau Solé, Ana Aguilera-Simón, Elena Jiménez-Xarrié, Alejandro Fernández-León, Mercedes Camacho, Marina Guasch-Jiménez, Rebeca Marin, Joan Martí-Fàbregas, Alejandro Martínez-Domeño, Luis Prats-Sánchez, Francesca Casoni, Belén Pérez, Francesc Jiménez-Altayó, Jose Luis Sánchez-Quesada and Sonia Benitez
Antioxidants 2023, 12(2), 438; https://0-doi-org.brum.beds.ac.uk/10.3390/antiox12020438 - 10 Feb 2023
Cited by 3 | Viewed by 1909
Abstract
Owing to the high risk of recurrence, identifying indicators of carotid plaque vulnerability in atherothrombotic ischemic stroke is essential. In this study, we aimed to identify modified LDLs and antioxidant enzymes associated with plaque vulnerability in plasma from patients with a recent ischemic [...] Read more.
Owing to the high risk of recurrence, identifying indicators of carotid plaque vulnerability in atherothrombotic ischemic stroke is essential. In this study, we aimed to identify modified LDLs and antioxidant enzymes associated with plaque vulnerability in plasma from patients with a recent ischemic stroke and carotid atherosclerosis. Patients underwent an ultrasound, a CT-angiography, and an 18F-FDG PET. A blood sample was obtained from patients (n = 64, 57.8% with stenosis ≥50%) and healthy controls (n = 24). Compared to the controls, patients showed lower levels of total cholesterol, LDL cholesterol, HDL cholesterol, apolipoprotein B (apoB), apoA-I, apoA-II, and apoE, and higher levels of apoJ. Patients showed lower platelet-activating factor acetylhydrolase (PAF-AH) and paraoxonase-1 (PON-1) enzymatic activities in HDL, and higher plasma levels of oxidized LDL (oxLDL) and electronegative LDL (LDL(−)). The only difference between patients with stenosis ≥50% and <50% was the proportion of LDL(−). In a multivariable logistic regression analysis, the levels of LDL(−), but not of oxLDL, were independently associated with the degree of carotid stenosis (OR: 5.40, CI: 1.15–25.44, p < 0.033), the presence of hypoechoic plaque (OR: 7.52, CI: 1.26–44.83, p < 0.027), and of diffuse neovessels (OR: 10.77, CI: 1.21–95.93, p < 0.033), indicating that an increased proportion of LDL(−) is associated with vulnerable atherosclerotic plaque. Full article
(This article belongs to the Special Issue Oxidative Stress and Inflammatory Mechanisms in Vascular Disorders)
Show Figures

Figure 1

17 pages, 4062 KiB  
Article
The Effect of Paracrine Factors Released by Irradiated Peripheral Blood Mononuclear Cells on Neutrophil Extracellular Trap Formation
by Katharina Klas, Anna S. Ondracek, Thomas M. Hofbauer, Andreas Mangold, Karin Pfisterer, Maria Laggner, Dragan Copic, Martin Direder, Daniel Bormann, Hendrik Jan Ankersmit and Michael Mildner
Antioxidants 2022, 11(8), 1559; https://0-doi-org.brum.beds.ac.uk/10.3390/antiox11081559 - 11 Aug 2022
Cited by 3 | Viewed by 2030
Abstract
Neutrophil extracellular trap (NET)-formation represents an important defence mechanism for the rapid clearance of infections. However, exaggerated NET formation has been shown to negatively affect tissue-regeneration after injury. As our previous studies revealed the strong tissue-protective and regenerative properties of the secretome of [...] Read more.
Neutrophil extracellular trap (NET)-formation represents an important defence mechanism for the rapid clearance of infections. However, exaggerated NET formation has been shown to negatively affect tissue-regeneration after injury. As our previous studies revealed the strong tissue-protective and regenerative properties of the secretome of stressed peripheral blood mononuclear cells (PBMCsec), we here investigated the influence of PBMCsec on the formation of NETs. The effect of PBMCsec on NET formation was assessed ex vivo in ionomycin stimulated neutrophils derived from healthy donors using flow cytometry, image stream analysis, and quantification of released extracellular DNA. The effect of PBMCsec on molecular mechanisms involved in NET formation, including Ca-flux, protein kinase C activity, reactive oxygen species production, and protein arginine deiminase 4 activity, were analysed. Our results showed that PBMCsec significantly inhibited NET formation. Investigation of the different biological substance classes found in PBMCsec revealed only a partial reduction in NET formation, suggesting a synergistic effect. Mechanistically, PBMCsec treatment did not interfere with calcium signalling and PKC-activation, but exerted anti-oxidant activity, as evidenced by reduced levels of reactive oxygen species and upregulation of heme oxygenase 1 and hypoxia inducible-factor 1 in PBMCsec-treated neutrophils. In addition, PBMCsec strongly inhibited the activation of protein arginine deiminase 4 (PAD4), ultimately leading to the inhibition of NET formation. As therapeutics antagonizing excessive NET formation are not currently available, our study provides a promising novel treatment option for a variety of conditions resulting from exaggerated NET formation. Full article
(This article belongs to the Special Issue Oxidative Stress and Inflammatory Mechanisms in Vascular Disorders)
Show Figures

Graphical abstract

Review

Jump to: Research

41 pages, 1232 KiB  
Review
Therapeutic Potential of Emerging NAD+-Increasing Strategies for Cardiovascular Diseases
by Noemi Rotllan, Mercedes Camacho, Mireia Tondo, Elena M. G. Diarte-Añazco, Marina Canyelles, Karen Alejandra Méndez-Lara, Sonia Benitez, Núria Alonso, Didac Mauricio, Joan Carles Escolà-Gil, Francisco Blanco-Vaca and Josep Julve
Antioxidants 2021, 10(12), 1939; https://0-doi-org.brum.beds.ac.uk/10.3390/antiox10121939 - 03 Dec 2021
Cited by 14 | Viewed by 5481
Abstract
Cardiovascular diseases are the leading cause of death worldwide. Aging and/or metabolic stress directly impact the cardiovascular system. Over the last few years, the contributions of altered nicotinamide adenine dinucleotide (NAD+) metabolism to aging and other pathological conditions closely related to cardiovascular diseases [...] Read more.
Cardiovascular diseases are the leading cause of death worldwide. Aging and/or metabolic stress directly impact the cardiovascular system. Over the last few years, the contributions of altered nicotinamide adenine dinucleotide (NAD+) metabolism to aging and other pathological conditions closely related to cardiovascular diseases have been intensively investigated. NAD+ bioavailability decreases with age and cardiometabolic conditions in several mammalian tissues. Compelling data suggest that declining tissue NAD+ is commonly related to mitochondrial dysfunction and might be considered as a therapeutic target. Thus, NAD+ replenishment by either genetic or natural dietary NAD+-increasing strategies has been recently demonstrated to be effective for improving the pathophysiology of cardiac and vascular health in different experimental models, as well as human health, to a lesser extent. Here, we review and discuss recent experimental evidence illustrating that increasing NAD+ bioavailability, particularly by the use of natural NAD+ precursors, may offer hope for new therapeutic strategies to prevent and treat cardiovascular diseases. Full article
(This article belongs to the Special Issue Oxidative Stress and Inflammatory Mechanisms in Vascular Disorders)
Show Figures

Graphical abstract

Back to TopTop