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Antioxidants
Special Issues
Oxidative Stress and Cardiovascular Disease
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Oxidative Stress and Cardiovascular Disease

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

Deadline for manuscript submissions: closed (30 September 2018) | Viewed by 23112

Special Issue Editors

Prof. Dr. Roberto Carnevale

E-Mail Website
Guest Editor
Department of Medical-Surgical Sciences and Biotechnologies, Sapienza University of Rome, 04100 Latina, Italy
Interests: NADPH oxidase; endothelial dysfunction; atherosclerosis
Special Issues, Collections and Topics in MDPI journals
Dr. Cristina Nocella

E-Mail Website
Guest Editor
Department of Clinical Internal, Anesthesiologic and Cardiovascular Sciences, Sapienza University of Rome, 00185 Rome, Italy
Interests: atherosclerosis; inflammation; oxidative stress; biomarkers; molecular mechanisms
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

The pathogenetic and prognostic roles of cardiovascular risk factors, such as hypercholesterolemia, arterial hypertension, diabetes mellitus, obesity, atrial fibrillation, advanced age, and smoking habits on cardiovascular (CV) outcomes are well established. Nevertheless, behind the classic mechanisms through which they contribute to accelerated cardiovascular events, in particular atherosclerosis, many studies have demonstrated that all these conditions are characterized by a common feature: Enhanced oxidative stress. When there is an imbalance between the elevated production of reactive oxygen species (ROS)/reactive nitrogen species (RNS) and missing antioxidants, there is an enhanced oxidative stress, leading to oxidative modifications of proteins, lipids, and DNA. The “oxidative stress theory” of cardiovascular disease is based on the assumption that the initial phase of disease is sustained by the increase in oxidative stress, dependent on ROS, produced both by blood cells and by resident cells of the arterial wall. Further investigation into this subject will provide renewed insight on the implication of oxidative stress in cardiovascular disease.

We are interested in original research articles, as well as review articles, that explore the mechanism insight and development of novel oxidative stress biomarkers, the development of strategies to treat these pathologies and the evaluation of outcomes, in particular using antioxidants drugs.

Potential topics include, but are not limited to:

  • Recent advances on the impact of oxidative stress in cardiovascular disease and atherosclerosis;
  • Redox signaling in the development of cardiac hypertrophy, remodeling and arrhythmias
  • Advances in epigenetics of CV diseases and atherosclerosis
  • Novel risk factors in cardiovascular diseases and latest advances in clinical evaluation
  • Elucidating the role of Oxidative Stress in Cardiovascular Inflammation
  • New molecules and biochemical pathways for the development of atherosclerotic plaque
  • microRNAs biology, their role in patho-physiology and therapy
Dr. Roberto Carnevale
Dr. Cristina Nocella
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
  • Cardiovascular disease
  • Atherosclerosis
  • Antioxidants
  • NADPH oxidase
  • Biomarkers
  • Epigenetics
  • Inflammation
  • Platelet function
  • Endothelial dysfunction

Published Papers (4 papers)

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Research

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10 pages, 1004 KiB  
Article
Interplay between Oxidative Stress and Platelet Activation in Coronary Thrombus of STEMI Patients
by Camilla Calvieri, Gaetano Tanzilli, Simona Bartimoccia, Roberto Cangemi, Alessio Arrivi, Marcello Dominici, Vittoria Cammisotto, Nicola Viceconte, Enrico Mangieri, Giacomo Frati and Francesco Violi
Antioxidants 2018, 7(7), 83; https://doi.org/10.3390/antiox7070083 - 03 Jul 2018
Cited by 17 | Viewed by 5758
Abstract
Background: Platelet activation and oxidative stress seem to play a key role in coronary thrombus formation and are associated with thrombus burden in ST-elevation myocardial infarction (STEMI). However, the interplay between oxidative stress and platelet activation has not been fully elucidated. Materials and [...] Read more.
Background: Platelet activation and oxidative stress seem to play a key role in coronary thrombus formation and are associated with thrombus burden in ST-elevation myocardial infarction (STEMI). However, the interplay between oxidative stress and platelet activation has not been fully elucidated. Materials and Methods: For 32 patients with STEMI undergoing primary percutaneous coronary intervention (PPCI) and 10 patients with stable angina (SA) and oxidative stress, as assessed by NADPH isoform 2 activity (soluble Nox2-derived peptide, sNox2-dp), levels of oxidized low-density lipoproteins (oxLDLs) and platelet activation markers such as soluble CD40 Ligand (sCD40L) and soluble P-selectin (sP-selectin) were measured in the retrieved material (coronary thrombi plus blood waste) of STEMI patients and in intracoronary blood of SA patients, respectively, and in peripheral blood samples of both groups. Results: In aspirated thrombi and blood waste of STEMI patients we found higher serum levels of sNox2-dp, oxLDLs, sCD40L, and sP-selectin, as compared to the intracoronary blood samples of SA patients. Moreover, in thrombi and blood waste of STEMI patients, a direct correlation between markers of oxidative stress and of platelet activation was found. Also, in STEMI patients a progressive increase of oxidative stress and platelet activation markers was observed according to the thrombus score burden. STEMI patients showed higher peripheral blood Nox2 activity and oxLDL levels as compared to SA patients. Conclusion: This study shows a close relationship between oxidative stress and platelet activation in the intracoronary blood waste and aspirated thrombi of STEMI patients, suggesting a role of oxidative stress in promoting thrombus formation and growth. Full article
(This article belongs to the Special Issue Oxidative Stress and Cardiovascular Disease)
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14 pages, 7842 KiB  
Article
High Glucose-Mediated Tyrosine Nitration of PI3-Kinase: A Molecular Switch of Survival and Apoptosis in Endothelial Cells
by Sally L. Elshaer, Tahira Lemtalsi and Azza B. El-Remessy
Antioxidants 2018, 7(4), 47; https://doi.org/10.3390/antiox7040047 - 25 Mar 2018
Cited by 13 | Viewed by 4806
Abstract
Diabetes and hyperglycemia are associated with increased retinal oxidative and nitrative stress and vascular cell death. Paradoxically, high glucose stimulates expression of survival and angiogenic growth factors. Therefore, we examined the hypothesis that high glucose-mediated tyrosine nitration causes inhibition of the survival protein [...] Read more.
Diabetes and hyperglycemia are associated with increased retinal oxidative and nitrative stress and vascular cell death. Paradoxically, high glucose stimulates expression of survival and angiogenic growth factors. Therefore, we examined the hypothesis that high glucose-mediated tyrosine nitration causes inhibition of the survival protein PI3-kinase, and in particular, its regulatory p85 subunit in retinal endothelial cell (EC) cultures. Retinal EC were cultured in high glucose (HG, 25 mM) for 3 days or peroxynitrite (PN, 100 µM) overnight in the presence or absence of a peroxynitrite decomposition catalyst (FeTPPs, 2.5 µM), or the selective nitration inhibitor epicatechin (100 µM). Apoptosis of ECs was assessed using TUNEL assay and caspase-3 activity. Immunoprecipitation and Western blot were used to assess protein expression and tyrosine nitration of p85 subunit and its interaction with the p110 subunit. HG or PN accelerated apoptosis of retinal ECs compared to normal glucose (NG, 5 mM) controls. HG- or PN-treated cells also showed significant increases in tyrosine nitration on the p85 subunit of PI3-kinase that inhibited its association with the catalytic p110 subunit and impaired PI3-kinase/Akt kinase activity. Decomposing peroxynitrite or blocking tyrosine nitration of p85 restored the activity of PI3-kinase, and prevented apoptosis and activation of p38 MAPK. Inhibiting p38 MAPK or overexpression of the constitutively activated Myr-Akt construct prevented HG- or peroxynitrite-mediated apoptosis. In conclusion, HG impairs pro-survival signals and causes accelerated EC apoptosis, at least in part via tyrosine nitration and inhibition of PI3-kinase. Inhibitors of nitration can be used in adjuvant therapy to delay diabetic retinopathy and microvascular complication. Full article
(This article belongs to the Special Issue Oxidative Stress and Cardiovascular Disease)
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Review

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20 pages, 1582 KiB  
Review
Cytoprotective Effects of Natural Compounds against Oxidative Stress
by Jay Mehta, Srujana Rayalam and Xinyu Wang
Antioxidants 2018, 7(10), 147; https://doi.org/10.3390/antiox7100147 - 20 Oct 2018
Cited by 59 | Viewed by 6578
Abstract
Oxidative stress, an imbalance between reactive oxygen species and antioxidants, has been witnessed in pathophysiological states of many disorders. Compounds identified from natural sources have long been recognized to ameliorate oxidative stress due to their inherent antioxidant activities. Here, we summarize the cytoprotective [...] Read more.
Oxidative stress, an imbalance between reactive oxygen species and antioxidants, has been witnessed in pathophysiological states of many disorders. Compounds identified from natural sources have long been recognized to ameliorate oxidative stress due to their inherent antioxidant activities. Here, we summarize the cytoprotective effects and mechanisms of natural or naturally derived synthetic compounds against oxidative stress. These compounds include: caffeic acid phenethyl ester (CAPE) found in honey bee propolis, curcumin from turmeric roots, resveratrol abundant in grape, and 1-[2-cyano-3,12-dioxooleana-1,9(11)-dien-28-oyl] imidazole (CDDO-Im), a synthetic triterpenoid based on naturally occurring oleanolic acid. Cytoprotective effects of these compounds in diseases conditions like cardiovascular diseases and obesity to decrease oxidative stress are discussed. Full article
(This article belongs to the Special Issue Oxidative Stress and Cardiovascular Disease)
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16 pages, 451 KiB  
Review
Oxidative Stress and Arterial Dysfunction in Peripheral Artery Disease
by Ahmed Ismaeel, Robert S. Brumberg, Jeffrey S. Kirk, Evlampia Papoutsi, Patrick J. Farmer, William T. Bohannon, Robert S. Smith, Jack L. Eidson, Ian Sawicki and Panagiotis Koutakis
Antioxidants 2018, 7(10), 145; https://doi.org/10.3390/antiox7100145 - 19 Oct 2018
Cited by 53 | Viewed by 5268
Abstract
Peripheral artery disease (PAD) is an atherosclerotic disease characterized by a narrowing of the arteries in the lower extremities. Disease manifestations are the result of more than just reduced blood flow, and include endothelial dysfunction, arterial stiffness, and inflammation. Growing evidence suggests that [...] Read more.
Peripheral artery disease (PAD) is an atherosclerotic disease characterized by a narrowing of the arteries in the lower extremities. Disease manifestations are the result of more than just reduced blood flow, and include endothelial dysfunction, arterial stiffness, and inflammation. Growing evidence suggests that these factors lead to functional impairment and decline in PAD patients. Oxidative stress also plays an important role in the disease, and a growing amount of data suggest a link between arterial dysfunction and oxidative stress. In this review, we present the current evidence for the involvement of endothelial dysfunction, arterial stiffness, and inflammation in the pathophysiology of PAD. We also discuss the links between these factors and oxidative stress, with a focus on nicotinamide adenine dinucleotide phosphate (NADPH) oxidase 2 (NOX2)-derived reactive oxygen species (ROS) and decreased nitric oxide (NO) bioavailability. Finally, the potential therapeutic role of NOX2 antioxidants for improving arterial function and functional status in PAD patients is explored. Full article
(This article belongs to the Special Issue Oxidative Stress and Cardiovascular Disease)
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