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Antioxidants
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Prevention of Atherosclerosis and of Low-Density Lipoprotein Oxidation: Role of...
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Prevention of Atherosclerosis and of Low-Density Lipoprotein Oxidation: Role of Dietary Antioxidant Compounds and Altered Redox Pathways. A Commemorative Special Issue in Honour of Professor Stanley Omaye

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

Deadline for manuscript submissions: 31 January 2025 | Viewed by 9659

Special Issue Editors

Prof. Dr. Alessandra Napolitano

E-Mail Website
Guest Editor
Department of Chemical Sciences, University of Naples “Federico II”, Via Cintia 4, I-80126 Naples, Italy
Interests: polyphenol antioxidants of dietary origin; conjugates of polyphenols with sulphydryl compounds of biological relevance; antioxidants from marine sources; valorization of agri food wastes; synthesis and exploitation of biopolymers from natural polyphenols; chemistry and structural investigation of natural polymers from catechols including human epidermal pigments melanins; oxidation chemistry of catecholamines in relation to neurodegenerative disorders; design and preparation of polydopamine related biomaterials with peculiar adhesive properties
Special Issues, Collections and Topics in MDPI journals
Dr. Mario Allegra

E-Mail Website
Guest Editor
Dipartimento di Scienze e Tecnologie Biologiche Chimiche e Farmaceutiche, Università degli Studi di Palermo, 90123 Palermo, Italy
Interests: eryptosis; antioxidants; oxidative stress; signaling patterns; inflammation; brain metabolism
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

The incidence of cardiovascular disease (CVD) increases markedly with age and is the largest contributor to morbidity and premature mortality in men and women. Increased levels of low-density lipoprotein (LDL) and free-radical-mediated oxidative damage of LDL represent a key risk factor and a key step in the pathogenesis of atherosclerosis. Indeed, oxidised LDL (oxLDL) plays a crucial role in the development of a chronic, low-grade inflammation state that strongly supports the evolution of CVD. Other mechanisms, including altered redox signalling and antioxidant pathways, may also be involved in the onset and development of these pathological conditions.

Approaches aimed at attenuating the risk of CVD, and which are based on dietary or supplemental antioxidants, have been increasingly investigated regarding the ability of different antioxidants and their combinations to protect LDL from oxidation. Other valuable strategies involve the targeting of altered redox signalling and the expression of antioxidant enzymes.

The research work developed by Professor Omaye and his collaborators has focused on nutraceuticals and their mode of action, particularly on antioxidant vitamins including ascorbate, alpha-tocopherol, and beta-carotene as protective agents against atherosclerosis and CVD. These vitamins have been shown to protect LDL against oxidative modification both in ex vivo supplementation studies and in vitro loading studies, suggesting that the protective effects against atherosclerosis associated with their intake may be mediated by their antioxidative activities.

This Special Issue dedicated to Professor Stanley Omaye will honour his memory, providing the latest insights into the actual role of antioxidants of dietary origin in the prevention of CVD, emerging from in vitro, animal studies and human trials. Altered redox mechanisms involved in CVD onset also represent a relevant and central topic of interest.

Original research papers, reviews and case studies addressing the topics reported below are herein welcome:

  • Studies aiming to investigate the mechanisms underlying the protective effects of antioxidants against oxLDL-related CVD;
  • Investigations into the ability of dietary antioxidants to counteract oxLDL-induced low-grade inflammation in CVD;
  • Epidemiological studies on the protective effects of dietary antioxidants against oxLDL-related CVD;
  • Studies on the bioavailability of dietary antioxidants;
  • Methodologies to investigate the action of antioxidants in experimental systems simulating LDL oxidation;
  • Investigations on redox signalling and altered antioxidant pathways related to CVD onset.

Prof. Dr. Alessandra Napolitano
Dr. Mario Allegra
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

  • LDL
  • oxidative stress
  • antioxidants
  • chronic, low-grade inflammation
  • vitamins
  • antioxidant enzymes
  • redox signalling

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Published Papers (4 papers)

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Research

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13 pages, 4705 KiB  
Article
PM2.5 Induces Cardiomyoblast Senescence via AhR-Mediated Oxidative Stress
by Tiantian Liu, Bin Jiang, Baoqiang Fu, Changyi Shang, Haobin Feng, Tao Chen and Yan Jiang
Antioxidants 2024, 13(7), 786; https://doi.org/10.3390/antiox13070786 - 28 Jun 2024
Cited by 3 | Viewed by 1066
Abstract
Previous research has established a correlation between PM2.5 exposure and aging-related cardiovascular diseases, primarily in blood vessels. However, the impact of PM2.5 on cardiomyocyte aging remains unclear. In this study, we observed that extractable organic matter (EOM) from PM2.5 exposure led to cellular [...] Read more.
Previous research has established a correlation between PM2.5 exposure and aging-related cardiovascular diseases, primarily in blood vessels. However, the impact of PM2.5 on cardiomyocyte aging remains unclear. In this study, we observed that extractable organic matter (EOM) from PM2.5 exposure led to cellular senescence in H9c2 cardiomyoblast cells, as characterized by an increase in the percentage of β-galactosidase-positive cells, elevated expression levels of p16 and p21, and enhanced H3K9me3 foci. EOM also induced cell cycle arrest at the G1/S stage, accompanied by downregulation of CDK4 and Cyclin D1. Furthermore, EOM exposure led to a significant elevation in intracellular reactive oxygen species (ROS), mitochondrial ROS, and DNA damage. Supplementation with the antioxidant NAC effectively attenuated EOM-induced cardiac senescence. Our findings also revealed that exposure to EOM activated the aryl hydrocarbon receptor (AhR) signaling pathway, as evidenced by AhR translocation to the nucleus and upregulation of Cyp1a1 and Cyp1b1. Importantly, the AhR antagonist CH223191 effectively mitigated EOM-induced oxidative stress and cellular senescence. In conclusion, our results indicate that PM2.5-induced AhR activation leads to oxidative stress, DNA damage, and cell cycle arrest, leading to cardiac senescence. Targeting the AhR/ROS axis might be a promising therapeutic strategy for combating PM2.5-induced cardiac aging. Full article
(This article belongs to the Special Issue Prevention of Atherosclerosis and of Low-Density Lipoprotein Oxidation: Role of Dietary Antioxidant Compounds and Altered Redox Pathways. A Commemorative Special Issue in Honour of Professor Stanley Omaye)
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Review

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26 pages, 1469 KiB  
Review
Facilitating Nitrite-Derived S-Nitrosothiol Formation in the Upper Gastrointestinal Tract in the Therapy of Cardiovascular Diseases
by Mila Silva-Cunha, Riccardo Lacchini and Jose E. Tanus-Santos
Antioxidants 2024, 13(6), 691; https://doi.org/10.3390/antiox13060691 - 4 Jun 2024
Viewed by 1219
Abstract
Cardiovascular diseases (CVDs) are often associated with impaired nitric oxide (NO) bioavailability, a critical pathophysiological alteration in CVDs and an important target for therapeutic interventions. Recent studies have revealed the potential of inorganic nitrite and nitrate as sources of NO, offering promising alternatives [...] Read more.
Cardiovascular diseases (CVDs) are often associated with impaired nitric oxide (NO) bioavailability, a critical pathophysiological alteration in CVDs and an important target for therapeutic interventions. Recent studies have revealed the potential of inorganic nitrite and nitrate as sources of NO, offering promising alternatives for managing various cardiovascular conditions. It is now becoming clear that taking advantage of enzymatic pathways involved in nitrite reduction to NO is very relevant in new therapeutics. However, recent studies have shown that nitrite may be bioactivated in the acidic gastric environment, where nitrite generates NO and a variety of S-nitrosating compounds that result in increased circulating S-nitrosothiol concentrations and S-nitrosation of tissue pharmacological targets. Moreover, transnitrosation reactions may further nitrosate other targets, resulting in improved cardiovascular function in patients with CVDs. In this review, we comprehensively address the mechanisms and relevant effects of nitrate and nitrite-stimulated gastric S-nitrosothiol formation that may promote S-nitrosation of pharmacological targets in various CVDs. Recently identified interfering factors that may inhibit these mechanisms and prevent the beneficial responses to nitrate and nitrite therapy were also taken into consideration. Full article
(This article belongs to the Special Issue Prevention of Atherosclerosis and of Low-Density Lipoprotein Oxidation: Role of Dietary Antioxidant Compounds and Altered Redox Pathways. A Commemorative Special Issue in Honour of Professor Stanley Omaye)
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32 pages, 1833 KiB  
Review
Radical Oxygen Species, Oxidized Low-Density Lipoproteins, and Lectin-like Oxidized Low-Density Lipoprotein Receptor 1: A Vicious Circle in Atherosclerotic Process
by Marco Munno, Alice Mallia, Arianna Greco, Gloria Modafferi, Cristina Banfi and Sonia Eligini
Antioxidants 2024, 13(5), 583; https://doi.org/10.3390/antiox13050583 - 9 May 2024
Cited by 4 | Viewed by 1718
Abstract
Atherosclerosis is a complex condition that involves the accumulation of lipids and subsequent plaque formation in the arterial intima. There are various stimuli, cellular receptors, and pathways involved in this process, but oxidative modifications of low-density lipoprotein (ox-LDL) are particularly important in the [...] Read more.
Atherosclerosis is a complex condition that involves the accumulation of lipids and subsequent plaque formation in the arterial intima. There are various stimuli, cellular receptors, and pathways involved in this process, but oxidative modifications of low-density lipoprotein (ox-LDL) are particularly important in the onset and progression of atherosclerosis. Ox-LDLs promote foam-cell formation, activate proinflammatory pathways, and induce smooth-muscle-cell migration, apoptosis, and cell death. One of the major receptors for ox-LDL is LOX-1, which is upregulated in several cardiovascular diseases, including atherosclerosis. LOX-1 activation in endothelial cells promotes endothelial dysfunction and induces pro-atherogenic signaling, leading to plaque formation. The binding of ox-LDLs to LOX-1 increases the generation of reactive oxygen species (ROS), which can induce LOX-1 expression and oxidize LDLs, contributing to ox-LDL generation and further upregulating LOX-1 expression. This creates a vicious circle that is amplified in pathological conditions characterized by high plasma levels of LDLs. Although LOX-1 has harmful effects, the clinical significance of inhibiting this protein remains unclear. Further studies both in vitro and in vivo are needed to determine whether LOX-1 inhibition could be a potential therapeutic target to counteract the atherosclerotic process. Full article
(This article belongs to the Special Issue Prevention of Atherosclerosis and of Low-Density Lipoprotein Oxidation: Role of Dietary Antioxidant Compounds and Altered Redox Pathways. A Commemorative Special Issue in Honour of Professor Stanley Omaye)
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19 pages, 1049 KiB  
Review
N-Acetylcysteine and Atherosclerosis: Promises and Challenges
by Yuqi Cui, Qiang Zhu, Hong Hao, Gregory C. Flaker and Zhenguo Liu
Antioxidants 2023, 12(12), 2073; https://doi.org/10.3390/antiox12122073 - 4 Dec 2023
Cited by 7 | Viewed by 4661
Abstract
Atherosclerosis remains a leading cause of cardiovascular diseases. Although the mechanism for atherosclerosis is complex and has not been fully understood, inflammation and oxidative stress play a critical role in the development and progression of atherosclerosis. N-acetylcysteine (NAC) has been used as a [...] Read more.
Atherosclerosis remains a leading cause of cardiovascular diseases. Although the mechanism for atherosclerosis is complex and has not been fully understood, inflammation and oxidative stress play a critical role in the development and progression of atherosclerosis. N-acetylcysteine (NAC) has been used as a mucolytic agent and an antidote for acetaminophen overdose with a well-established safety profile. NAC has antioxidant and anti-inflammatory effects through multiple mechanisms, including an increase in the intracellular glutathione level and an attenuation of the nuclear factor kappa-B mediated production of inflammatory cytokines like tumor necrosis factor-alpha and interleukins. Numerous animal studies have demonstrated that NAC significantly decreases the development and progression of atherosclerosis. However, the data on the outcomes of clinical studies in patients with atherosclerosis have been limited and inconsistent. The purpose of this review is to summarize the data on the effect of NAC on atherosclerosis from both pre-clinical and clinical studies and discuss the potential mechanisms of action of NAC on atherosclerosis, as well as challenges in the field. Full article
(This article belongs to the Special Issue Prevention of Atherosclerosis and of Low-Density Lipoprotein Oxidation: Role of Dietary Antioxidant Compounds and Altered Redox Pathways. A Commemorative Special Issue in Honour of Professor Stanley Omaye)
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