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Antioxidants
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Oxidative Stress in Cardiovascular Diseases (CVDs)
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Oxidative Stress in Cardiovascular Diseases (CVDs)

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: 10 June 2025 | Viewed by 10006

Special Issue Editors

Dr. Roberto Palacios-Ramirez

E-Mail Website
Guest Editor
Unidad de Excelencia Instituto de Biomedicina y Genética Molecular (IBGM), Universidad de Valladolid—Centro Superior de Investigaciones Cientificas (CSIC), 47003 Valladolid, Spain
Interests: kidney disease; cardiovascular diseases; oxidative stress; inflammation
Dr. Ernesto Martínez-Martínez

E-Mail Website
Guest Editor
Physiology Department, School of Medicine, Universidad Complutense, 28040 Madrid, Spain
Interests: cardiovascular disease; renal research; biomarkers; mitochondrial dysfunction
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Reactive oxygen species (ROS) are well-known mediators of the molecular biology of cells. ROS are key to maintaining several functions such as hearing or host defense and are second messengers of many signaling pathways in physiological conditions. In the organism, there are several ROS-producing systems. These systems are counterbalanced with ROS-scavenging systems. In some situations, either due to an overproduction of ROS or a defect in the ROS clearance, this balance is broken. In this scenario, ROS start to accumulate, leading to oxidative stress.

Oxidative stress has been associated with many pathophysiological processes, including cardiovascular diseases. Different overactivated ROS sources such as the mitochondrion, NADPH oxidase, xanthine oxidase, or cyclooxygenase-2 are involved in the development and maintenance of diseases such as hypertension, atherosclerosis, heart failure, stroke, or diabetes.

This Special Issue of Antioxidants entitled "Oxidative Stress in Cardiovascular Diseases (CVDs)" aims to provide a close look at the current research on the role of oxidative stress in cardiovascular pathologies. Original research articles and reviews addressing the gaps in the knowledge of the mechanisms triggered by the accumulation of ROS and the subsequent effect on the organism, including end-organ damage, in cardiovascular pathologies are welcome.

We look forward to your contributions.

Dr. Roberto Palacios-Ramirez
Dr. Ernesto Martínez-Martínez
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

  • ROS
  • oxidative stress
  • antioxidants
  • cardiovascular diseases

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Published Papers (4 papers)

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Review

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31 pages, 1295 KiB  
Review
Oxidative Stress and Cardiovascular Complications in Type 2 Diabetes: From Pathophysiology to Lifestyle Modifications
by Alfredo Caturano, Maria Rocco, Giuseppina Tagliaferri, Alessia Piacevole, Davide Nilo, Giovanni Di Lorenzo, Ilaria Iadicicco, Mariarosaria Donnarumma, Raffaele Galiero, Carlo Acierno, Celestino Sardu, Vincenzo Russo, Erica Vetrano, Caterina Conte, Raffaele Marfella, Luca Rinaldi and Ferdinando Carlo Sasso
Antioxidants 2025, 14(1), 72; https://doi.org/10.3390/antiox14010072 - 9 Jan 2025
Viewed by 970
Abstract
Type 2 diabetes mellitus (T2DM) is a chronic metabolic disorder that significantly increases the risk of cardiovascular disease, which is the leading cause of morbidity and mortality among diabetic patients. A central pathophysiological mechanism linking T2DM to cardiovascular complications is oxidative stress, defined [...] Read more.
Type 2 diabetes mellitus (T2DM) is a chronic metabolic disorder that significantly increases the risk of cardiovascular disease, which is the leading cause of morbidity and mortality among diabetic patients. A central pathophysiological mechanism linking T2DM to cardiovascular complications is oxidative stress, defined as an imbalance between reactive oxygen species (ROS) production and the body’s antioxidant defenses. Hyperglycemia in T2DM promotes oxidative stress through various pathways, including the formation of advanced glycation end products, the activation of protein kinase C, mitochondrial dysfunction, and the polyol pathway. These processes enhance ROS generation, leading to endothelial dysfunction, vascular inflammation, and the exacerbation of cardiovascular damage. Additionally, oxidative stress disrupts nitric oxide signaling, impairing vasodilation and promoting vasoconstriction, which contributes to vascular complications. This review explores the molecular mechanisms by which oxidative stress contributes to the pathogenesis of cardiovascular disease in T2DM. It also examines the potential of lifestyle modifications, such as dietary changes and physical activity, in reducing oxidative stress and mitigating cardiovascular risks in this high-risk population. Understanding these mechanisms is critical for developing targeted therapeutic strategies to improve cardiovascular outcomes in diabetic patients. Full article
(This article belongs to the Special Issue Oxidative Stress in Cardiovascular Diseases (CVDs))
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46 pages, 6077 KiB  
Review
Mitochondrial Reactive Oxygen Species Dysregulation in Heart Failure with Preserved Ejection Fraction: A Fraction of the Whole
by Caroline Silveira Martinez, Ancheng Zheng and Qingzhong Xiao
Antioxidants 2024, 13(11), 1330; https://doi.org/10.3390/antiox13111330 - 31 Oct 2024
Cited by 1 | Viewed by 1833
Abstract
Heart failure with preserved ejection fraction (HFpEF) is a multifarious syndrome, accounting for over half of heart failure (HF) patients receiving clinical treatment. The prevalence of HFpEF is rapidly increasing in the coming decades as the global population ages. It is becoming clearer [...] Read more.
Heart failure with preserved ejection fraction (HFpEF) is a multifarious syndrome, accounting for over half of heart failure (HF) patients receiving clinical treatment. The prevalence of HFpEF is rapidly increasing in the coming decades as the global population ages. It is becoming clearer that HFpEF has a lot of different causes, which makes it challenging to find effective treatments. Currently, there are no proven treatments for people with deteriorating HF or HFpEF. Although the pathophysiologic foundations of HFpEF are complex, excessive reactive oxygen species (ROS) generation and increased oxidative stress caused by mitochondrial dysfunction seem to play a critical role in the pathogenesis of HFpEF. Emerging evidence from animal models and human myocardial tissues from failed hearts shows that mitochondrial aberrations cause a marked increase in mitochondrial ROS (mtROS) production and oxidative stress. Furthermore, studies have reported that common HF medications like beta blockers, angiotensin receptor blockers, angiotensin-converting enzyme inhibitors, and mineralocorticoid receptor antagonists indirectly reduce the production of mtROS. Despite the harmful effects of ROS on cardiac remodeling, maintaining mitochondrial homeostasis and cardiac functions requires small amounts of ROS. In this review, we will provide an overview and discussion of the recent findings on mtROS production, its threshold for imbalance, and the subsequent dysfunction that leads to related cardiac and systemic phenotypes in the context of HFpEF. We will also focus on newly discovered cellular and molecular mechanisms underlying ROS dysregulation, current therapeutic options, and future perspectives for treating HFpEF by targeting mtROS and the associated signal molecules. Full article
(This article belongs to the Special Issue Oxidative Stress in Cardiovascular Diseases (CVDs))
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19 pages, 988 KiB  
Review
Effects of Heart Failure Therapies on Atrial Fibrillation: Biological and Clinical Perspectives
by Alfredo Mauriello, Antonia Ascrizzi, Anna Selvaggia Roma, Riccardo Molinari, Alfredo Caturano, Egidio Imbalzano, Antonello D’Andrea and Vincenzo Russo
Antioxidants 2024, 13(7), 806; https://doi.org/10.3390/antiox13070806 - 2 Jul 2024
Cited by 2 | Viewed by 1587
Abstract
Heart failure (HF) and atrial fibrillation (AF) are prevalent cardiovascular diseases that contribute significantly to morbidity, mortality, hospitalisation, and healthcare costs. It is not uncommon for these conditions to coexist and have mutually reinforcing effects. A critical factor in the aetiology of these [...] Read more.
Heart failure (HF) and atrial fibrillation (AF) are prevalent cardiovascular diseases that contribute significantly to morbidity, mortality, hospitalisation, and healthcare costs. It is not uncommon for these conditions to coexist and have mutually reinforcing effects. A critical factor in the aetiology of these conditions is oxidative stress, driven by reactive oxygen species (ROS), which contributes to atrial remodelling and fibrosis. The recent introduction of new drugs for the treatment of heart failure has also had an impact on the management of atrial fibrillation due to their influence on oxidative stress. The objective of this review is to analyse the effects of these therapies, including their role in mitigating ROS, on the prevention and treatment of AF in HF patients. Full article
(This article belongs to the Special Issue Oxidative Stress in Cardiovascular Diseases (CVDs))
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Other

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19 pages, 3062 KiB  
Systematic Review
Eicosapentaenoic Acid (EPA) and Docosahexaenoic Acid (DHA) Ameliorate Heart Failure through Reductions in Oxidative Stress: A Systematic Review and Meta-Analysis
by Jayant Seth, Sohat Sharma, Cameron J. Leong and Simon W. Rabkin
Antioxidants 2024, 13(8), 955; https://doi.org/10.3390/antiox13080955 - 6 Aug 2024
Viewed by 4851
Abstract
The objectives of this study were to explore the role that eicosapentaenoic acid (EPA) and/or docosahexaenoic acid (DHA) plays in heart failure (HF), highlighting the potential connection to oxidative stress pathways. Following PRISMA guidelines, we conducted electronic searches of the literature in MEDLINE [...] Read more.
The objectives of this study were to explore the role that eicosapentaenoic acid (EPA) and/or docosahexaenoic acid (DHA) plays in heart failure (HF), highlighting the potential connection to oxidative stress pathways. Following PRISMA guidelines, we conducted electronic searches of the literature in MEDLINE and EMBASE focusing on serum EPA and/or DHA and EPA and/or DHA supplementation in adult patients with heart failure or who had heart failure as an outcome of this study. We screened 254 studies, encompassing RCTs, observational studies, and cohort studies that examined HF outcomes in relation to either serum concentrations or dietary supplementation of EPA and/or DHA. The exclusion criteria were pediatric patients, non-HF studies, abstracts, editorials, case reports, and reviews. Eleven studies met our criteria. In meta-analyses, high serum concentrations of DHA were associated with a lower rate of heart failure with a hazard ratio of 0.74 (CI = 0.59–0.94). High serum concentrations of EPA also were associated with an overall reduction in major adverse cardiovascular events with a hazard ratio of 0.60 (CI = 0.46–0.77). EPA and DHA, or n3-PUFA administration, were associated with an increased LVEF with a mean difference of 1.55 (CI = 0.07–3.03)%. A potential explanation for these findings is the ability of EPA and DHA to inhibit pathways by which oxidative stress damages the heart or impairs cardiac systolic or diastolic function producing heart failure. Specifically, EPA may lower oxidative stress within the heart by reducing the concentration of reactive oxygen species (ROS) within cardiac tissue by (i) upregulating nuclear factor erythroid 2-related factor 2 (Nrf2), which increases the expression of antioxidant enzyme activity, including heme oxygenase-1, thioredoxin reductase 1, ferritin light chain, ferritin heavy chain, and manganese superoxide dismutase (SOD), (ii) increasing the expression of copper–zinc superoxide dismutase (MnSOD) and glutathione peroxidase, (iii) targeting Free Fatty Acid Receptor 4 (Ffar4), (iv) upregulating expression of heme-oxygenase-1, (v) lowering arachidonic acid levels, and (vi) inhibiting the RhoA/ROCK signaling pathway. DHA may lower oxidative stress within the heart by (i) reducing levels of mitochondrial-fission-related protein DRP-1(ser-63), (ii) promoting the incorporation of cardiolipin within the mitochondrial membrane, (iii) reducing myocardial fibrosis, which leads to diastolic heart failure, (iv) reducing the expression of genes such as Appa, Myh7, and Agtr1α, and (v) reducing inflammatory cytokines such as IL-6, TNF-α. In conclusion, EPA and/or DHA have the potential to improve heart failure, perhaps mediated by their ability to modulate oxidative stress. Full article
(This article belongs to the Special Issue Oxidative Stress in Cardiovascular Diseases (CVDs))
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