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Antioxidants
Special Issues
Understanding Oxidative Stress in Cardiovascular Disorders
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Understanding Oxidative Stress in Cardiovascular Disorders

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 March 2025) | Viewed by 2725

Special Issue Editors

Dr. Matteo Becatti

E-Mail Website
Guest Editor
Department of Experimental and Clinical Biomedical Sciences "Mario Serio", University of Firenze, 50121 Firenze, Italy
Interests: thrombosis; fibrinogen; oxidative stress; protein structure
Special Issues, Collections and Topics in MDPI journals
Dr. Claudia Fiorillo

E-Mail Website
Guest Editor
Department of Biomedical, Experimental and Clinical Sciences “Mario Serio”, University of Florence, Viale Morgagni 50, 50134 Florence, Italy
Interests: redox markers; antioxidant capacity; post-translational oxidative modification; ROS sources
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

We are pleased to introduce our forthcoming Special Issue, which will delve into the critical relationship between oxidative stress and cardiovascular diseases (CVDs). Oxidative stress, characterized by an imbalance between reactive oxygen species (ROS) production and the body's antioxidant defenses, has emerged as a central player in the pathogenesis and progression of various cardiovascular disorders.

This Special Issue aims to illuminate the intricate mechanisms through which oxidative stress contributes to the development and exacerbation of CVDs, including atherosclerosis, hypertension, myocardial infarction, and heart failure. By unraveling the involved molecular pathways, we seek to identify novel therapeutic targets and interventions to combat these debilitating conditions.

Contributions to this Special Issue will explore the multifaceted roles of oxidative stress in CVDs, from its impact on endothelial dysfunction and vascular inflammation to its involvement in myocardial remodeling and cardiac dysfunction. Researchers are encouraged to investigate both the upstream triggers of oxidative stress, such as dyslipidemia, hypertension, and diabetes, as well as the downstream consequences, including the oxidative modification of lipids, proteins, and DNA.

Furthermore, we welcome studies that explore the potential of antioxidant therapies and lifestyle interventions in mitigating oxidative stress and preventing CVDs. From preclinical research elucidating the efficacy of novel antioxidants to clinical trials evaluating the cardiovascular benefits of dietary modifications and exercise interventions, this Special Issue aims to provide a comprehensive overview of current strategies for managing oxidative stress in the context of cardiovascular health.

In summary, this Special Issue seeks to advance our understanding of the complex interplay between oxidative stress and cardiovascular diseases. By identifying key molecular targets and therapeutic strategies, we aim to pave the way for innovative approaches to prevent, diagnose, and treat CVDs, ultimately improving patient outcomes and reducing the global burden of cardiovascular morbidity and mortality.

Dr. Matteo Becatti
Dr. Claudia Fiorillo
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
  • reactive oxygen species
  • cardiovascular diseases
  • antioxidants
  • diet
  • exercise

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Further information on MDPI's Special Issue policies can be found here.

Published Papers (3 papers)

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Research

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15 pages, 2453 KiB  
Article
TNFα Induces DNA and Histone Hypomethylation and Pulmonary Artery Smooth Muscle Cell Proliferation Partly via Excessive Superoxide Formation
by Patrick Crosswhite and Zhongjie Sun
Antioxidants 2024, 13(6), 677; https://doi.org/10.3390/antiox13060677 - 31 May 2024
Cited by 1 | Viewed by 1163
Abstract
Objective: The level of tumor necrosis factor-α (TNF-α) is upregulated during the development of pulmonary vascular remodeling and pulmonary hypertension. A hallmark of pulmonary arterial (PA) remodeling is the excessive proliferation of PA smooth muscle cells (PASMCs). The purpose of this study is [...] Read more.
Objective: The level of tumor necrosis factor-α (TNF-α) is upregulated during the development of pulmonary vascular remodeling and pulmonary hypertension. A hallmark of pulmonary arterial (PA) remodeling is the excessive proliferation of PA smooth muscle cells (PASMCs). The purpose of this study is to investigate whether TNF-α induces PASMC proliferation and explore the potential mechanisms. Methods: PASMCs were isolated from 8-week-old male Sprague-Dawley rats and treated with 0, 20, or 200 ng/mL TNF-α for 24 or 48 h. After treatment, cell number, superoxide production, histone acetylation, DNA methylation, and histone methylation were assessed. Results: TNF-α treatment increased NADPH oxidase activity, superoxide production, and cell numbers compared to untreated controls. TNF-α-induced PASMC proliferation was rescued by a superoxide dismutase mimetic tempol. TNF-α treatment did not affect histone acetylation at either dose but did significantly decrease DNA methylation. DNA methyltransferase 1 activity was unchanged by TNF-α treatment. Further investigation using QRT-RT-PCR revealed that GADD45-α, a potential mediator of DNA demethylation, was increased after TNF-α treatment. RNAi inhibition of GADD45-α alone increased DNA methylation. TNF-α impaired the epigenetic mechanism leading to DNA hypomethylation, which can be abolished by a superoxide scavenger tempol. TNF-α treatment also decreased H3-K4 methylation. TNF-α-induced PASMC proliferation may involve the H3-K4 demethylase enzyme, lysine-specific demethylase 1 (LSD1). Conclusions: TNF-α-induced PASMC proliferation may be partly associated with excessive superoxide formation and histone and DNA methylation. Full article
(This article belongs to the Special Issue Understanding Oxidative Stress in Cardiovascular Disorders)
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Review

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29 pages, 2958 KiB  
Review
Relevance of Targeting Oxidative Stress, Inflammatory, and Pro-Resolution Mechanisms in the Prevention and Management of Postoperative Atrial Fibrillation
by Abir Attia, Kalai Mangai Muthukumarasamy, Doa’a G. F. Al-U’Datt and Roddy Hiram
Antioxidants 2025, 14(4), 414; https://doi.org/10.3390/antiox14040414 - 29 Mar 2025
Viewed by 433
Abstract
Atrial fibrillation (AF) is the most common cardiac arrhythmia. AF can lead to severe complications, including stroke, myocardial infarction, and sudden death. AF risk factors include pathological aging and conditions such as obesity, diabetes, and hypertension. Clinical data revealed that cardiothoracic and non-cardiothoracic [...] Read more.
Atrial fibrillation (AF) is the most common cardiac arrhythmia. AF can lead to severe complications, including stroke, myocardial infarction, and sudden death. AF risk factors include pathological aging and conditions such as obesity, diabetes, and hypertension. Clinical data revealed that cardiothoracic and non-cardiothoracic surgeries are also important risk factors for AF. Post-operative AF (POAF) is associated with important public health costs caused by increased hospitalization, frequent emergency room visits, and enhanced healthcare utilization, which altogether lead to a low quality of life for the patients. Hence, POAF is a major clinical challenge, and there is an urgent need for the development of novel therapeutic strategies. Interestingly, evidence from clinical and fundamental research converges to identify cardiac oxidative stress and atrial inflammation as the common denominators of all AF risk factors. Unresolved inflammation is suspected to provoke cardiac fibrosis, which is an important contributor to cardiac arrhythmias and AF. Antioxidant, anti-inflammatory, and pro-resolution strategies may help to combat post-operative cardiac remodeling and POAF. This article aims to review the current scientific evidence supporting the role of inflammation in the pathogenesis of POAF and explore potential novel therapeutic strategies to prevent and mitigate inflammation in the management of AF. Full article
(This article belongs to the Special Issue Understanding Oxidative Stress in Cardiovascular Disorders)
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33 pages, 1249 KiB  
Review
Fibrinogen Oxidation and Thrombosis: Shaping Structure and Function
by Francesca Nencini, Elvira Giurranna, Serena Borghi, Niccolò Taddei, Claudia Fiorillo and Matteo Becatti
Antioxidants 2025, 14(4), 390; https://doi.org/10.3390/antiox14040390 - 26 Mar 2025
Viewed by 346
Abstract
Fibrinogen, a pivotal plasma glycoprotein, plays an essential role in hemostasis by serving as the precursor to fibrin, which forms the structural framework of blood clots. Beyond coagulation, fibrinogen influences immune responses, inflammation, and tissue repair. Oxidative stress, characterized by an imbalance between [...] Read more.
Fibrinogen, a pivotal plasma glycoprotein, plays an essential role in hemostasis by serving as the precursor to fibrin, which forms the structural framework of blood clots. Beyond coagulation, fibrinogen influences immune responses, inflammation, and tissue repair. Oxidative stress, characterized by an imbalance between reactive oxygen species (ROS) and antioxidants, induces fibrinogen oxidation, significantly altering its structure and function. This narrative review synthesizes findings from in vitro, ex vivo, and clinical studies, emphasizing the impact of fibrinogen oxidation on clot formation, architecture, and degradation. Oxidative modifications result in denser fibrin clots with thinner fibers, reduced permeability, and heightened resistance to fibrinolysis. These structural changes exacerbate prothrombotic conditions in cardiovascular diseases, diabetes, chronic inflammatory disorders and cancer. In contrast, “low-dose” oxidative stress may elicit protective adaptations in fibrinogen, preserving its function. The review also highlights discrepancies in experimental findings due to variability in oxidation protocols and patient conditions. Understanding the interplay between oxidation and fibrinogen function could unveil therapeutic strategies targeting oxidative stress. Antioxidant therapies or selective inhibitors of detrimental oxidation hold potential for mitigating thrombotic risks. However, further research is essential to pinpoint specific fibrinogen oxidation sites, clarify their roles in clot dynamics, and bridge the gap between basic research and clinical practice. Full article
(This article belongs to the Special Issue Understanding Oxidative Stress in Cardiovascular Disorders)
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