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Antioxidants
Special Issues
Redox Biology and Cardiovascular Disease
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Redox Biology and Cardiovascular 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 January 2021) | Viewed by 12583

Special Issue Editors

Prof. Dr. Eric E. Kelley

E-Mail Website
Guest Editor
Department of Physiology and Pharmacology, West Virginia University, School of Medicine, Morgantown, WV, USA
Interests: redox signaling in obesity and diabetes; xanthine oxidase (pathobiology, regulation and biochemistry) nitric oxide; vascular responses to oxidant stress and oxidant/antioxidant interaction
Dr. Adam C. Straub

E-Mail Website
Guest Editor
Department of Pharmacology and Chemical Biology, Vascular Medicine Institute, University of Pittsburgh, Pittsburgh, PA, USA
Interests: cardiovascular redox signaling; nitric oxide; oxidants; vascular wall biology; hypertension; heart failure; sickle cell disease

Special Issue Information

Dear Colleagues,

As you are all keenly aware, cardiovascular disease remains an important issue worldwide. At the core of the pathobiology in numerous processes ultimately driving poor cardiovascular outcomes is the elevated rates of oxidant generation in the face of diminished capacity for small molecular weight antioxidants and antioxidant enzyme systems. Intimately linked to this interplay between oxidants and antioxidants is inflammation; yet it remains unclear whether oxidant load or inflammation is the seminal driver (the chicken or egg conundrum). Recent advances in our capacity to more specifically identify reactive species and their downstream metabolites, genetic tools and advanced imaging has served to move the field forward and identify novel targets for therapeutic approaches to address numerous cardiovascular disease processes; however, many goals are yet to be accomplished. As such, this Special Issue aims to collect papers which deal with all aspects of redox-related processes involved in the etiology, propagation and resolution of cardiovascular disease. Contributions describing recent developments in redox signalling and the identification of novel targets/pathways are particularly welcome.

Prof. Dr. Eric E. Kelley
Dr. Adam C. Straub
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

  • oxidants
  • cardiovascular
  • nitric oxide
  • inflammation
  • oxidases
  • antioxidants
  • redox signaling
  • vascular homeostasis
  • redox reactions

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Published Papers (3 papers)

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Research

14 pages, 9066 KiB  
Article
Extra-Nuclear Functions of the Transcription Factor Grainyhead-Like 3 in the Endothelium—Interaction with Endothelial Nitric Oxide Synthase
by Kirsten Jander, Jan Greulich, Stefanie Gonnissen, Niloofar Ale-Agha, Christine Goy, Philipp Jakobs, Sabrina Farrokh, Corina Marziano, Swapnil K. Sonkusare, Judith Haendeler and Joachim Altschmied
Antioxidants 2021, 10(3), 428; https://doi.org/10.3390/antiox10030428 - 11 Mar 2021
Cited by 3 | Viewed by 2459
Abstract
We previously demonstrated that the transcription factor Grainyhead-like 3 (GRHL3) has essential functions in endothelial cells by inhibiting apoptosis and promoting migration as well as activation of endothelial nitric oxide synthase (eNOS). We now show that a large portion of the protein is [...] Read more.
We previously demonstrated that the transcription factor Grainyhead-like 3 (GRHL3) has essential functions in endothelial cells by inhibiting apoptosis and promoting migration as well as activation of endothelial nitric oxide synthase (eNOS). We now show that a large portion of the protein is localized to myo-endothelial projections of murine arteries suggesting extra-nuclear functions. Therefore, we generated various deletion mutants to identify the nuclear localization signal (NLS) of GRHL3 and assessed potential extra-nuclear functions. Several large-scale deletion mutants were incapable of activating a GRHL3-dependent reporter construct, which could either be due to deficiencies in transcriptional activation or to impaired nuclear import. One of these mutants encompassed a predicted bipartite NLS whose deletion led to the retention of GRHL3 outside the nucleus. Interestingly, this mutant retained functions of the full-length protein as it could still inhibit pathways inducing endothelial cell apoptosis. As apoptosis protection by GRHL3 depends on NO-production, we examined whether GRHL3 could interact with eNOS and showed a direct interaction, which was enhanced with the extra-nuclear GRHL3 variant. The observation that endogenous GRHL3 also interacts with eNOS in intact murine arteries corroborated these findings and substantiated the notion that GRHL3 has important extra-nuclear functions in the endothelium. Full article
(This article belongs to the Special Issue Redox Biology and Cardiovascular Disease)
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22 pages, 9268 KiB  
Article
Oxidatively Modified LDL Suppresses Lymphangiogenesis via CD36 Signaling
by Bhupesh Singla, Hui-Ping Lin, WonMo Ahn, Joseph White and Gábor Csányi
Antioxidants 2021, 10(2), 331; https://doi.org/10.3390/antiox10020331 - 23 Feb 2021
Cited by 13 | Viewed by 4741
Abstract
Arterial accumulation of plasma-derived LDL and its subsequent oxidation contributes to atherosclerosis. Lymphatic vessel (LV)-mediated removal of arterial cholesterol has been shown to reduce atherosclerotic lesion formation. However, the precise mechanisms that regulate LV density and function in atherosclerotic vessels remain to be [...] Read more.
Arterial accumulation of plasma-derived LDL and its subsequent oxidation contributes to atherosclerosis. Lymphatic vessel (LV)-mediated removal of arterial cholesterol has been shown to reduce atherosclerotic lesion formation. However, the precise mechanisms that regulate LV density and function in atherosclerotic vessels remain to be identified. The aim of this study was to investigate the role of native LDL (nLDL) and oxidized LDL (oxLDL) in modulating lymphangiogenesis and underlying molecular mechanisms. Western blotting and immunostaining experiments demonstrated increased oxLDL expression in human atherosclerotic arteries. Furthermore, elevated oxLDL levels were detected in the adventitial layer, where LV are primarily present. Treatment of human lymphatic endothelial cells (LEC) with oxLDL inhibited in vitro tube formation, while nLDL stimulated it. Similar results were observed with Matrigel plug assay in vivo. CD36 deletion in mice and its siRNA-mediated knockdown in LEC prevented oxLDL-induced inhibition of lymphangiogenesis. In addition, oxLDL via CD36 receptor suppressed cell cycle, downregulated AKT and eNOS expression, and increased levels of p27 in LEC. Collectively, these results indicate that oxLDL inhibits lymphangiogenesis via CD36-mediated regulation of AKT/eNOS pathway and cell cycle. These findings suggest that therapeutic blockade of LEC CD36 may promote arterial lymphangiogenesis, leading to increased cholesterol removal from the arterial wall and reduced atherosclerosis. Full article
(This article belongs to the Special Issue Redox Biology and Cardiovascular Disease)
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16 pages, 2727 KiB  
Article
Anti-Atherogenic Effects of Orlistat on Obesity-Induced Vascular Oxidative Stress Rat Model
by Zaidatul Akmal Othman, Zaida Zakaria, Joseph Bagi Suleiman, Wan Syaheedah Wan Ghazali and Mahaneem Mohamed
Antioxidants 2021, 10(2), 251; https://doi.org/10.3390/antiox10020251 - 6 Feb 2021
Cited by 37 | Viewed by 4800
Abstract
Obesity is typically linked to oxidative stress and inflammation, which lead to vascular damage and initiate the progression of atherosclerosis. The aim of this study was to determine the anti-atherosclerotic effect of orlistat on obesity-induced vascular oxidative stress in obese male rats. Twenty-four [...] Read more.
Obesity is typically linked to oxidative stress and inflammation, which lead to vascular damage and initiate the progression of atherosclerosis. The aim of this study was to determine the anti-atherosclerotic effect of orlistat on obesity-induced vascular oxidative stress in obese male rats. Twenty-four male Sprague–Dawley rats were categorized into two groups: normal (Normal group, n = 6) and high-fat diet (HFD group, n = 12). After six weeks, obese rats in the HFD group were administered either with distilled water (OB group) or orlistat 10 mg/kg/day (OB/OR group) for another six weeks. The OB group had a significant increase in lipid profiles (total cholesterol (TC), triglyceride (TG), low-density lipoprotein (LDL)) and decrease in high-density lipoprotein (HDL) level compared to the Normal group. The aortic antioxidants enzymes activities (superoxide dismutase (SOD), glutathione peroxidase (GPx), glutathione reductase (GR), glutathione S-transferase (GST), and catalase (CAT)) as well as total glutathione (GSH) and total antioxidant capacity (TAC) of the OB group were significantly decreased compared to the Normal group. Furthermore, pro-inflammatory atherosclerotic markers (tumour necrosis factor-alpha (TNF-α), vascular cell adhesion molecule-1 (VCAM-1), and intercellular cell adhesion molecule-1 (ICAM-1)) expressions were increased significantly, and anti-inflammatory marker (interleukin-10 (IL-10)) was decreased significantly in the OB group compared to the Normal group. Treatment with orlistat significantly improved lipid profile, increased antioxidant enzymes and expression of anti-inflammatory markers, and decreased the expression of the pro-inflammatory marker compared to the OB group. These findings may suggest the therapeutic effect of orlistat in attenuating the progression of the atherosclerotic stage in obesity. Full article
(This article belongs to the Special Issue Redox Biology and Cardiovascular Disease)
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