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Roles of Vascular Oxidative Stress in the Pathogenesis of Atherosclerosis
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Roles of Vascular Oxidative Stress in the Pathogenesis of Atherosclerosis

A special issue of Journal of Clinical Medicine (ISSN 2077-0383). This special issue belongs to the section "Vascular Medicine".

Deadline for manuscript submissions: closed (20 December 2019) | Viewed by 35817

Special Issue Editor

Prof. Dr. Victor M. Victor

E-Mail Website
Guest Editor
1. FISABIO–Hospital Universitario Dr. Peset, Valencia, Spain
2. Centro de Investigación Biomédica en Red de Enfermedades Hepáticas y Digestivas (CIBERehd), Valencia, Spain
3. Departamento de Fisiología, Facultad de Medicina, Universidad de Valencia, Valencia, Spain
Interests: mitochondria; autophagy; type 2 diabetes; oxidative stress; mitophagy; insulin resistance; atherosclerosis
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

It is well known that reactive oxygen species (ROS) and oxidative stress are related to the pathogenesis of atherosclerosis and cardiovascular diseases (CVD). Atherosclerosis represents a state of exacerbated oxidative stress characterized by protein and lipid oxidation in the vascular endothelium. Similarly, endothelial dysfunction is also characterized by a loss of nitric oxide (NO) bioactivity, which occurs early on in the development of atherosclerosis and can determine the development of future vascular complications. In general, ROS are essential to cell functions, including redox signaling, proliferation of cells, and mitogenesis, and can mimic and amplify the action of growth factors; at the same time, adequate levels of antioxidant defenses are required in order to avoid the harmful effects of excessive ROS production.

Therefore, it is clear that the biological specificity of ROS action depends on the localization, amount, and duration of ROS production. To date, although major ROS-sensitive signal transduction pathways have been shown to be involved in atherosclerosis, there is still much to be learned about their mutual interaction and the modifications they undergo during metabolic and vascular diseases, including type 2 diabetes. Due to the relevance of such topics, it would seem appropriate to summarize some of the main recent advances in research on the role of vascular oxidative stress in the pathogenesis of atherosclerosis and its impact on health, disease and aging.
We invite authors to submit original articles and review articles on this interesting topic.
Potential topics include, but are not limited, to the following:

  • Role of ROS in atherosclerosis
  • Type 2 diabetes and atherosclerosis
  • Signaling pathways of ROS action
  • Positive feedback loop in ROS production
  • Interaction among cellular sources of ROS production
  • New insight into the relationship between oxidative stress and atherosclerosis
  • Role of oxidative stress in metabolic, cardiovascular diseases and cancer.
  • Vascular oxidative stress and autophagy-mitophagy
  • Vascular oxidative stress and reticulum stress

Dr. Victor M Victor
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. Journal of Clinical Medicine is an international peer-reviewed open access semimonthly 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 2600 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

  • Atherosclerosis
  • Vascular
  • Oxidative stress
  • Mitochondria
  • Mitophagy
  • Autophagy
  • Type 2 diabetes

Published Papers (4 papers)

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Research

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27 pages, 2594 KiB  
Article
Marine Polyhydroxynaphthoquinone, Echinochrome A: Prevention of Atherosclerotic Inflammation and Probable Molecular Targets
by Aleksandr A. Artyukov, Elena A. Zelepuga, Larisa N. Bogdanovich, Natalia M. Lupach, Vyacheslav L. Novikov, Tatyana A. Rutckova and Emma P. Kozlovskaya
J. Clin. Med. 2020, 9(5), 1494; https://doi.org/10.3390/jcm9051494 - 15 May 2020
Cited by 19 | Viewed by 3395
Abstract
The effect of low doses of echinochrome A (EchA), a natural polyhydroxy-1,4-naphthoquinone pigment from the sea urchin Scaphechinus mirabilis, has been studied in clinical trials, when it was used as an active substance of the drug Histochrome® and biologically active supplement [...] Read more.
The effect of low doses of echinochrome A (EchA), a natural polyhydroxy-1,4-naphthoquinone pigment from the sea urchin Scaphechinus mirabilis, has been studied in clinical trials, when it was used as an active substance of the drug Histochrome® and biologically active supplement Thymarin. Several parameters of lipid metabolism, antioxidant status, and the state of the immune system were analyzed in patients with cardiovascular diseases (CVD), including contaminating atherosclerosis. It has been shown that EchA effectively normalizes lipid metabolism, recovers antioxidant status and reduces atherosclerotic inflammation, regardless of the method of these preparations’ administrations. Treatment of EchA has led to the stabilization of patients, improved function of the intracellular matrix and decreased epithelial dysfunction. The increased expression of surface human leukocyte antigen DR isotype (HLA-DR) receptors reflects the intensification of intercellular cooperation of immune cells, as well as an increase in the efficiency of processing and presentation of antigens, while the regulation of CD95 + expression levels suggests the stimulation of cell renewal processes. The immune system goes to a different level of functioning. Computer simulations suggest that EchA, with its aromatic structure of the naphthoquinone nucleus, may be a suitable ligand of the cytosolic aryl cell receptor, which affects the response of the immune system and causes the rapid expression of detoxification enzymes such as CYP and DT diaphorase, which play a protective role with CVD. Therefore, EchA possesses not only an antiradical effect and antioxidant activity, but is also a SOD3 mimetic, producing hydrogen peroxide and controlling the expression of cell enzymes through hypoxia-inducible factors (HIF), peroxisome proliferator-activated receptors (PPARs) and aryl hydrocarbon receptor (AhR). Full article
(This article belongs to the Special Issue Roles of Vascular Oxidative Stress in the Pathogenesis of Atherosclerosis)
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11 pages, 1072 KiB  
Article
The SGLT2 Inhibitor Empagliflozin Ameliorates the Inflammatory Profile in Type 2 Diabetic Patients and Promotes an Antioxidant Response in Leukocytes
by Francesca Iannantuoni, Aranzazu M. de Marañon, Noelia Diaz-Morales, Rosa Falcon, Celia Bañuls, Zaida Abad-Jimenez, Victor M. Victor, Antonio Hernandez-Mijares and Susana Rovira-Llopis
J. Clin. Med. 2019, 8(11), 1814; https://doi.org/10.3390/jcm8111814 - 01 Nov 2019
Cited by 92 | Viewed by 5187
Abstract
Sodium–glucose co-transporter 2 inhibitors (iSGLT2) have been linked to a considerable reduction in cardiovascular risk in patients with type 2 diabetes (T2D), but the precise molecular mechanisms are still elusive. We aimed to evaluate the effects of the iSGLT2 empagliflozin on systemic inflammation [...] Read more.
Sodium–glucose co-transporter 2 inhibitors (iSGLT2) have been linked to a considerable reduction in cardiovascular risk in patients with type 2 diabetes (T2D), but the precise molecular mechanisms are still elusive. We aimed to evaluate the effects of the iSGLT2 empagliflozin on systemic inflammation and its potential antioxidant properties. This is an observational, prospective follow-up study of a cohort of fifteen patients with T2D who received 10 mg/day of empagliflozin according to standard clinical care. Measures at baseline, 12 and 24 weeks were taken. Metabolic and anthropometric parameters were evaluated. Production of mitochondrial superoxide, glutathione content, and glutathione s-reductase and catalase mRNA levels were measured in leukocytes. Serum levels of myeloperoxidase, hs-CRP and IL-10 were determined. In addition to decreased body weight and reduced glucose and HbA1c levels, we observed a reduction in superoxide production in leukocytes of diabetic patients and increased glutathione content, prominently after 24 weeks of empagliflozin treatment. Leukocyte expression of glutathione s-reductase and catalase, and serum levels of IL-10 were enhanced at 24 weeks of empagliflozin treatment. Concomitantly, reduced hs-CRP and myeloperoxidase levels were seen. This study provides evidence of the antioxidant and anti-inflammatory properties of empagliflozin treatment in humans, which may contribute to its beneficial cardiovascular effects. Full article
(This article belongs to the Special Issue Roles of Vascular Oxidative Stress in the Pathogenesis of Atherosclerosis)
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19 pages, 11354 KiB  
Article
The Mitochondrial Antioxidant SS-31 Modulates Oxidative Stress, Endoplasmic Reticulum Stress, and Autophagy in Type 2 Diabetes
by Irene Escribano-López, Aranzazu M de Marañon, Francesca Iannantuoni, Sandra López-Domènech, Zaida Abad-Jiménez, Pedro Díaz, Eva Solá, Nadezda Apostolova, Milagros Rocha and Víctor M Víctor
J. Clin. Med. 2019, 8(9), 1322; https://doi.org/10.3390/jcm8091322 - 28 Aug 2019
Cited by 25 | Viewed by 4198
Abstract
Mitochondrial dysfunction has been shown to play a central role in the pathophysiology of type 2 diabetes (T2D), and mitochondria-targeted agents such as SS-31 are emerging as a promising strategy for its treatment. We aimed to study the effects of SS-31 on leukocytes [...] Read more.
Mitochondrial dysfunction has been shown to play a central role in the pathophysiology of type 2 diabetes (T2D), and mitochondria-targeted agents such as SS-31 are emerging as a promising strategy for its treatment. We aimed to study the effects of SS-31 on leukocytes from T2D patients by evaluating oxidative stress, endoplasmic reticulum (ER) stress and autophagy. Sixty-one T2D patients and 53 controls were included. Anthropometric and analytical measurements were performed. We also assessed reactive oxygen species (ROS) production, calcium content, the expression of ER stress markers GRP78, CHOP, P-eIF2α, and autophagy-related proteins Beclin1, LC3 II/I, and p62 in leukocytes from T2D and control subjects treated or not with SS-31. Furthermore, we have evaluated the action of SS-31 on leukocyte-endothelium interactions. T2D patients exhibited elevated ROS concentration, calcium levels and presence of ER markers (GRP78 and CHOP gene expression, and GRP78 and P-eIF2α protein expression), all of which were reduced by SS-31 treatment. SS-31 also led to a drop in BECN1 gene expression, and Beclin1 and LC3 II/I protein expression in T2D patients. In contrast, the T2D group displayed reduced p62 protein levels that were restored by SS-31. SS-20 (with non-antioxidant activity) did not change any analyzed parameter. In addition, SS-31 decreased rolling flux and leukocyte adhesion, and increased rolling velocity in T2D patients. Our findings suggest that SS-31 exerts potentially beneficial effects on leukocytes of T2D patients modulating oxidative stress and autophagy, and ameliorating ER stress. Full article
(This article belongs to the Special Issue Roles of Vascular Oxidative Stress in the Pathogenesis of Atherosclerosis)
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Review

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22 pages, 3008 KiB  
Review
Relationship between Oxidative Stress, ER Stress, and Inflammation in Type 2 Diabetes: The Battle Continues
by Estefania Burgos-Morón, Zaida Abad-Jiménez, Aranzazu Martínez de Marañón, Francesca Iannantuoni, Irene Escribano-López, Sandra López-Domènech, Christian Salom, Ana Jover, Vicente Mora, Ildefonso Roldan, Eva Solá, Milagros Rocha and Víctor M. Víctor
J. Clin. Med. 2019, 8(9), 1385; https://doi.org/10.3390/jcm8091385 - 04 Sep 2019
Cited by 320 | Viewed by 22513
Abstract
Type 2 diabetes (T2D) is a metabolic disorder characterized by hyperglycemia and insulin resistance in which oxidative stress is thought to be a primary cause. Considering that mitochondria are the main source of ROS, we have set out to provide a general overview [...] Read more.
Type 2 diabetes (T2D) is a metabolic disorder characterized by hyperglycemia and insulin resistance in which oxidative stress is thought to be a primary cause. Considering that mitochondria are the main source of ROS, we have set out to provide a general overview on how oxidative stress is generated and related to T2D. Enhanced generation of reactive oxygen species (ROS) and oxidative stress occurs in mitochondria as a consequence of an overload of glucose and oxidative phosphorylation. Endoplasmic reticulum (ER) stress plays an important role in oxidative stress, as it is also a source of ROS. The tight interconnection between both organelles through mitochondrial-associated membranes (MAMs) means that the ROS generated in mitochondria promote ER stress. Therefore, a state of stress and mitochondrial dysfunction are consequences of this vicious cycle. The implication of mitochondria in insulin release and the exposure of pancreatic β-cells to hyperglycemia make them especially susceptible to oxidative stress and mitochondrial dysfunction. In fact, crosstalk between both mechanisms is related with alterations in glucose homeostasis and can lead to the diabetes-associated insulin-resistance status. In the present review, we discuss the current knowledge of the relationship between oxidative stress, mitochondria, ER stress, inflammation, and lipotoxicity in T2D. Full article
(This article belongs to the Special Issue Roles of Vascular Oxidative Stress in the Pathogenesis of Atherosclerosis)
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