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New Insight into Redox Homeostasis and Oxidative Stress in Health and Disease: Focus on Cardiac and Vascular Function

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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: 30 October 2026 | Viewed by 7758

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Special Issue Editors

Prof. Dr. István Szokodi

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Guest Editor

Heart Institute, Medical School, University of Pécs, 7624 Pécs, Hungary
Interests: cardiokines; exerkines; cardiac contractility; vascular tone; exercise-induced adaptation in cardiac and skeletal muscles; heart failure; cell signaling

Prof. Dr. Endre Sulyok

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Guest Editor

National Laboratory for Human Reproduction, University of Pécs, 7624 Pecs, Hungary
Interests: perinatal adaptation; human reproduction; in vitro fertilization; reproductive endocrinology; reproductive aging; biomarkers; endothelial dysfunction
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Special Issue Information

Dear Colleagues,

Reactive oxygen species (ROS) and reactive nitrogen species (RNS) play a fundamental role in maintaining cardiovascular homeostasis through redox signaling mechanisms that regulate vascular tone, myocardial function, metabolic adaptation, and cell growth and survival, among other processes. Under physiological conditions, ROS/RNS signaling is subject to tight spatiotemporal regulation and is intimately integrated into metabolic networks. However, the dysregulation of these processes can shift cellular homeostasis towards oxidative or nitrosative stress, promoting endothelial dysfunction, inflammation, fibrosis, cellular senescence, and cell death, as observed in cardiovascular diseases such as atherosclerosis, hypertension, stroke, myocardial infarction, and heart failure. Clinical trials indiscriminately suppressing ROS/RNS pathways have yielded inconsistent results, highlighting the challenge of selectively modulating redox balance without disrupting essential physiological signaling. Furthermore, the paucity of research in areas such as sex-specific redox dynamics, genetically determined redox profiles, ROS/RNS interactions with metabolic pathways, and the absence of reliable, actionable biomarkers for patient stratification or therapy monitoring suggests additional avenues for investigation. The objective of this Special Issue is to promote this paradigm shift, which may entail the transformation of redox-based interventions into clinically effective strategies for the prevention and treatment of cardiovascular disease. We invite you to submit your latest research findings or a review article to this Special Issue.

Prof. Dr. István Szokodi
Prof. Dr. Endre Sulyok
Guest Editors

Manuscript Submission Information

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Keywords

reactive oxygen/nitrogen species
oxidative/nitrosative stress
redox signaling
atherosclerosis
hypertension
stroke
myocardial infarction
heart failure
biomarker
translational and precision medicine

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Published Papers (5 papers)

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Research

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15 pages, 2384 KB

Open AccessArticle

Antagonizing IL-17A Reduces Vascular Inflammation and Attenuates Oxidative Stress Formation but Does Not Significantly Improve Vascular Dysfunction Induced by One Week of Angiotensin II Treatment

by Rebecca Jung, Annika Lehmann, Tanja Knopp, Michael Molitor, Katharina Perius, Jens Posma, Venkata Garlapati, Thomas Münzel, Andreas Daiber, Philipp Lurz, Philip Wenzel, Ari Waisman, Johannes Wild and Susanne Helena Karbach

Antioxidants 2026, 15(2), 229; https://doi.org/10.3390/antiox15020229 - 10 Feb 2026

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Abstract

Introduction: The pro-inflammatory cytokine interleukin-17A (IL-17A) has a key role in the inflammatory cascade and promotes vascular inflammation and dysfunction. In addition, IL-17A is centrally involved in several autoimmune diseases. IL-17A deficiency has been linked to reduced vascular inflammation associated with attenuated arterial hypertension under long-term angiotensin II (Ang II) exposure for four weeks. This is of interest as IL-17A is one factor linking several autoimmune diseases with cardiovascular comorbidity. So far, little is known about the effects of IL-17A during the early stages of vascular dysfunction development—an interval possibly representing an optimal therapeutic window. Methods: Mice lacking the IL-17A receptor alpha (IL-17RAdel) and wild-type counterparts were treated with Ang II for one week (1 mg/kg bodyweight/week). We assessed systemic oxidative stress formation and vascular function, as well as inflammatory cells in the vessel wall. In parallel, C57BL/6J mice treated with Ang II received anti-IL-17A therapy, to evaluate the same parameters. Results: Both IL-17RA-deficient mice and anti-IL-17A-treated C57BL/6J mice exhibited an attenuated oxidative stress response and mitigated vascular inflammation following one week of Ang II treatment. These effects did not significantly prevent the onset of Ang II-induced vascular dysfunction at that timepoint. Conclusions: After one week of Ang II treatment, antagonizing IL-17RA or IL-17A only partially reduced/attenuated the Ang II-induced effects on the vasculature. In the context of IL-17A-driven autoimmune diseases with associated vascular pathology, our findings suggest that anti-inflammatory therapies alone may not be sufficient to attenuate vascular impairment. A combined approach including agents with direct protective vascular effects may be required for effective intervention for the associated vascular comorbidity. Full article

(This article belongs to the Special Issue New Insight into Redox Homeostasis and Oxidative Stress in Health and Disease: Focus on Cardiac and Vascular Function)

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21 pages, 11644 KB

Open AccessArticle

Heme as a Pro-Inflammatory Stimulus in Abdominal Aortic Aneurysm

by Yuchao Ding, László Potor, Péter Sótonyi, Ágnes Szappanos, Gergő Péter Gyurok, Szilárd Póliska, Andreas Patsalos, Gábor Méhes, Lívia Beke, Katalin Éva Sikura, Erzsébet Zavaczki, Tamás Gáll, Dávid Pethő, Attila Fintha, Beáta Nagy, Béla Juhász, László Nagy, György Balla and József Balla

Antioxidants 2026, 15(2), 155; https://doi.org/10.3390/antiox15020155 - 23 Jan 2026

Cited by 1 | Viewed by 892

Abstract

Abdominal aortic aneurysm (AAA) is a lethal vascular disease characterized by intramural hemorrhage. This study delineates the signatures of heme and its metabolic imbalance related to progression and inflammation in AAA. Clinical analyses of patients undergoing open AAA surgery show that AAA patients exhibit vascular inflammation, with elevated serum CRP, IL-6, and heme levels correlating with the expression of heme-regulated gene Hmox1/HO-1 (heme oxygenase-1) in the affected aortic wall. Oxidation of hemoglobin to ferri state leading to accumulation of methemoglobin readily releasing heme occurs in human AAA and in angiotensin II (AngII)-induced AAA in apolipoprotein E-deficient mice. Transcriptomic analysis for AngII-induced AAA identifies upregulated genes predominantly enriched in inflammatory signaling, extracellular matrix degradation, oxidative stress pathways, and altered expression of genes related to heme metabolism including Hmox1. Immunohistochemistry for IL1β and TNFα confirms inflammatory activation within AAA tissues. The signatures of heme-responsive gene inductions, enhanced expression of HO-1 and H-ferritin, are detected. Mechanistic studies employing endothelial cells and smooth muscle cells reveal that heme exposure of resident cells markedly enhances the expression of IL1β and ICAM1, as well as the inflammasome component NLRP3, and such inflammatory response is controlled by HO-1. Intervention with Normosang (heme arginate), an HO-1 inducer, attenuates aneurysm progression, whereas HO-1 inhibition by Tin protoporphyrin IX abolishes this protection. Induction of HO-1 accompanied by elevated H-ferritin level also mitigated aortic wall inflammation as reflected by lowering IL1β and TNFα. These findings highlight the heme-HO-1-H-ferritin axis as an element of AAA pathogenesis and a potential therapeutic target. Full article

(This article belongs to the Special Issue New Insight into Redox Homeostasis and Oxidative Stress in Health and Disease: Focus on Cardiac and Vascular Function)

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16 pages, 1714 KB

Open AccessArticle

Temporal Exercise Conditioning Confers Dual-Phase Cardioprotection Against Isoproterenol-Induced Injury in a Rat Model

by Krisztina Kupai, Zsolt Murlasits, Hsu Lin Kang, Eszter Regős, Ákos Várkonyi, Csaba Lengyel, Imre Pávó, Zsolt Radák, Béla Juhász, Dániel Priksz and Anikó Pósa

Antioxidants 2026, 15(2), 152; https://doi.org/10.3390/antiox15020152 - 23 Jan 2026

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Abstract

Exercise training has demonstrated potential benefits in addressing the adverse effects of cardiovascular diseases, particularly myocardial infarction (MI). This study analyzed the cardioprotective effects of moderate exercise before and after MI in rats subjected to isoproterenol (ISO)-induced heart damage. Wistar rats were assigned to five groups: controls (CTRL), isoproterenol-treated (ISO), swimming before ISO (PRE + ISO), swimming after ISO (ISO + POST), and swimming both before and after ISO (PRE + ISO + POST). Cardiac function was assessed through echocardiography, while oxidative stress markers, Heme Oxygenase-1 (HO-1) and Myeloperoxidase (MPO), were quantified using biochemical assays and enzyme-linked immunosorbent assay (ELISA). Statistical analyses were conducted by one-way analysis of variance (ANOVA), accompanied by Tukey’s post hoc test. Exercise performed post-MI and both pre- and post-MI significantly reduced ISO-induced infarct size and improved left ventricular function (stroke volume (SV), ejection fraction (EF), and Tei index). HO-1 protein concentration and HO enzyme activity were restored, while swim training reduced the activity of MPO compared to the ISO group. Moderate exercise training, when appropriately timed, provides cardioprotection against ISO-induced myocardial damage by reducing oxidative stress and cardiac dysfunction. Full article

(This article belongs to the Special Issue New Insight into Redox Homeostasis and Oxidative Stress in Health and Disease: Focus on Cardiac and Vascular Function)

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Review

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17 pages, 2007 KB

Open AccessReview

Modulation of Redox-Sensitive Cardiac Ion Channels

by Razan Orfali, Al Hassan Gamal El-Din, Varnika Karthick, Elisanjer Lamis, Vanna Xiao, Alena Ramanishka, Abdullah Alwatban, Osama Alkhamees, Ali Alaseem, Young-Woo Nam and Miao Zhang

Antioxidants 2025, 14(7), 836; https://doi.org/10.3390/antiox14070836 - 8 Jul 2025

Cited by 6 | Viewed by 2578

Abstract

Redox regulation is crucial for the cardiac action potential, coordinating the sodium-driven depolarization, calcium-mediated plateau formation, and potassium-dependent repolarization processes required for proper heart function. Under physiological conditions, low-level reactive oxygen species (ROS), generated by mitochondria and membrane oxidases, adjust ion channel function and support excitation–contraction coupling. However, when ROS accumulate, they modify a variety of important channel proteins in cardiomyocytes, which commonly results in reducing potassium currents, enhancing sodium and calcium influx, and enhancing intracellular calcium release. These redox-driven alterations disrupt the cardiac rhythm, promote after-depolarizations, impair contractile force, and accelerate the development of heart diseases. Experimental models demonstrate that oxidizing agents reduce repolarizing currents, whereas reducing systems restore normal channel activity. Similarly, oxidative modifications of calcium-handling proteins amplify sarcoplasmic reticulum release and diastolic calcium leak. Understanding the precise redox-dependent modifications of cardiac ion channels would guide new possibilities for targeted therapies aimed at restoring electrophysiological homeostasis under oxidative stress, potentially alleviating myocardial infarction and cardiovascular dysfunction. Full article

(This article belongs to the Special Issue New Insight into Redox Homeostasis and Oxidative Stress in Health and Disease: Focus on Cardiac and Vascular Function)

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17 pages, 1092 KB

Open AccessReview

Takotsubo Syndrome and Oxidative Stress: Physiopathological Linkage and Future Perspectives

by Alfredo Mauriello, Carmen Del Giudice, Gerardo Elia Del Vecchio, Adriana Correra, Anna Chiara Maratea, Martina Grieco, Arianna Amata, Vincenzo Quagliariello, Nicola Maurea, Riccardo Proietti, Antonio Giordano, Antonello D’Andrea and Vincenzo Russo

Antioxidants 2025, 14(5), 522; https://doi.org/10.3390/antiox14050522 - 27 Apr 2025

Cited by 10 | Viewed by 2171

Abstract

Takotsubo syndrome (TTS) is an acute coronary syndrome of unknown prevalence with a physiopathological mechanism that is not yet fully understood. The course is generally benign. Current therapeutic management is based on limited evidence. Oxidative stress seems to play a role in the pathogenesis of cardiovascular diseases, especially regarding the endothelial dysfunction underlying TTS. The present review aims to describe the pathophysiological mechanisms linking oxidative stress and TTS, explore the impact of oxidative stress on TTS, and evaluate the efficacy of anti-oxidative stress therapies on TTS. Full article

(This article belongs to the Special Issue New Insight into Redox Homeostasis and Oxidative Stress in Health and Disease: Focus on Cardiac and Vascular Function)

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