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Oxidative Stress and Inflammation in Cardiovascular Diseases - 3rd Edition

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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: closed (15 February 2024) | Viewed by 18576

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Dr. Raelene Pickering

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Department of Diabetes, Central Clinical School, Monash University, Melbourne 3800, Australia
Interests: atherosclerosis; renin-angiotensin aldosterone system; RNA splicing; inflammation; molecular biology; immunology; diabetic complications
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Dr. Arpeeta Sharma

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Department of Diabetes, Central Clinical School, Monash University, Melbourne 3800, Australia
Interests: diabetes-associated cardiovascular complications

Special Issue Information

Dear Colleagues,

Cardiovascular diseases are the leading cause of death worldwide, with risk factors such as diabetes, high blood pressure, and obesity increasing the prevalence of disease. Oxidative stress and inflammation are intricately linked mechanisms and are significant drivers in the development and progression of cardiovascular disease. Although reactive oxygen species are a natural by-product of metabolism, oxidative stress occurs when there is a build-up of reactive oxygen species that are unable to be scavenged by the available intracellular antioxidants. Oxidative stress leads to damaged DNA, protein, and lipids. Additionally, increased oxidative stress activates several inflammatory pathways, resulting in the production of inflammatory cytokines that damage the cardiovascular system. Given the increased burden of cardiovascular diseases, there is a clear need to develop a better understanding of the mechanisms underlying oxidative stress and inflammation in these diseases. This will aid in the development of more targeted and effective treatment strategies as well as provide advances that will lead to tangible outcomes in improving diagnosis. Furthermore, the importance of understanding cardiovascular diseases has been further highlighted this past year during the pandemic where they predict a greater chance of morbidity and mortality among COVID-19-infected individuals.

In this Special Issue, our aim is to summarize the current understanding of cardiovascular complications, highlighting the novel and innovative work being carried out.

Dr. Raelene Pickering
Dr. Arpeeta Sharma
Guest Editors

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Keywords

oxidative stress
reductive stress
inflammatory cytokines
cardiovascular injury
cardiovascular pathology
inflammation

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Published Papers (10 papers)

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Research

22 pages, 26274 KiB

Open AccessArticle

Anti-Ferroptotic Treatment Deteriorates Myocardial Infarction by Inhibiting Angiogenesis and Altering Immune Response

by Rebecca A. Stairley, Allison M. Trouten, Shuang Li, Patrick L. Roddy, Kristine Y. DeLeon-Pennell, Kyu-Ho Lee, Henry M. Sucov, Chun Liu and Ge Tao

Antioxidants 2024, 13(7), 769; https://doi.org/10.3390/antiox13070769 - 26 Jun 2024

Viewed by 2378

Abstract

Mammalian cardiomyocytes have limited regenerative ability. Cardiac disease, such as congenital heart disease and myocardial infarction, causes an initial loss of cardiomyocytes through regulated cell death (RCD). Understanding the mechanisms that govern RCD in the injured myocardium is crucial for developing therapeutics to promote heart regeneration. We previously reported that ferroptosis, a non-apoptotic and iron-dependent form of RCD, is the main contributor to cardiomyocyte death in the injured heart. To investigate the mechanisms underlying the preference for ferroptosis in cardiomyocytes, we examined the effects of anti-ferroptotic reagents in infarcted mouse hearts. The results revealed that the anti-ferroptotic reagent did not improve neonatal heart regeneration, and further compromised the cardiac function of juvenile hearts. On the other hand, ferroptotic cardiomyocytes played a supportive role during wound healing by releasing pro-angiogenic factors. The inhibition of ferroptosis in the regenerating mouse heart altered the immune and angiogenic responses. Our study provides insights into the preference for ferroptosis over other types of RCD in stressed cardiomyocytes, and guidance for designing anti-cell-death therapies for treating heart disease. Full article

(This article belongs to the Special Issue Oxidative Stress and Inflammation in Cardiovascular Diseases - 3rd Edition)

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12 pages, 2158 KiB

Open AccessCommunication

The Role of NOX2-Derived Reactive Oxygen Species in the Induction of Endothelin-Converting Enzyme-1 by Angiotensin II

by Michael Adu-Gyamfi, Claudia Goettsch, Julian Kamhieh-Milz, Lei Chen, Anna Maria Pfefferkorn, Anja Hofmann, Coy Brunssen, Gregor Müller, Thomas Walther, Muhammad Imtiaz Ashraf, Henning Morawietz, Janusz Witowski and Rusan Catar

Antioxidants 2024, 13(4), 500; https://doi.org/10.3390/antiox13040500 - 22 Apr 2024

Cited by 1 | Viewed by 1293

Abstract

Endothelin-1 is a key regulator of vascular tone and blood pressure in health and disease. We have recently found that ET-1 production in human microvascular endothelial cells (HMECs) can be promoted by angiotensin II (Ang II) through a novel mechanism involving octamer-binding transcription factor-1 (Oct-1), NADPH oxidase-2 (NOX2), and superoxide anions. As the formation of bioactive ET-1 also depends on endothelin-converting enzyme-1 (ECE-1), we investigated the transcriptional regulation of the ECE1 gene. We found that exposure of HMECs to Ang II resulted in a concentration- and time-dependent increase in ECE1 mRNA expression. Pharmacological inhibition of ECE-1 reduced Ang II-stimulated ET-1 release to baseline values. The effect of Ang II on ECE1 mRNA expression was associated with Oct-1 binding to the ECE1 promoter, resulting in its increased activity. Consequently, the Ang II-stimulated increase in ECE1 mRNA expression could be prevented by siRNA-mediated Oct-1 inhibition. It could also be abolished by silencing the NOX2 gene and neutralizing superoxide anions with superoxide dismutase. In mice fed a high-fat diet, cardiac expression of Ece1 mRNA increased in wild-type mice but not in Nox2-deficient animals. It can be concluded that Ang II engages Oct-1, NOX2, and superoxide anions to stimulate ECE1 expression in the endothelium. Full article

(This article belongs to the Special Issue Oxidative Stress and Inflammation in Cardiovascular Diseases - 3rd Edition)

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14 pages, 870 KiB

Open AccessArticle

Systemic Oxidative Stress in Subacute Stroke Patients Undergoing Rehabilitation Treatment

by Carola Cocco, Mariacristina Siotto, Alessandro Guerrini, Marco Germanotta, Caterina Galluccio, Valeria Cipollini, Laura Cortellini, Arianna Pavan, Stefania Lattanzi, Sabina Insalaco, Elisabetta Ruco, Rita Mosca, Biagio Campana and Irene Aprile

Antioxidants 2024, 13(3), 354; https://doi.org/10.3390/antiox13030354 - 15 Mar 2024

Viewed by 1559

Abstract

The imbalance in oxidative stress in acute stroke has been extensively studied; on the contrary, its investigation in the subacute phase is limited. The aim of this study was to analyse the variation in the systemic oxidative status in subacute post-stroke patients before (T0) and after a six-week rehabilitation treatment (T1) and to investigate the relationship between systemic oxidative status and rehabilitation outcomes. We enrolled 109 subjects in two different centres, and we analysed their serum hydroperoxide levels (d-ROMs), biological antioxidant power (BAP), thiol antioxidant components (-SHp), and relative antioxidant capacity (OSI and SH-OSI indices). Activity of Daily Living (ADL), hand grip strength, and walking endurance were evaluated using the modified Barthel Index, the Hand Grip test, and the 6-min walk test, respectively. At T0, most of the patients showed very high levels of d-ROMs and suboptimal levels of the BAP, OSI, and SH-OSI indices. Comparing the T1 and T0 data, we observed an improvement in the rehabilitation outcomes and a significant decrease in d-ROMs (549 ± 126 vs. 523 ± 148, p = 0.023), as well as an improvement in the OSI and SH-OSI indices (4.3 ± 1.3 vs. 4.7 ± 1.5, p = 0.001; 11.0 ± 0.4 vs. 1.2 ± 0.4, p < 0.001). In addition, significant correlations were seen between the oxidative stress parameters and the rehabilitation outcomes. These results suggest monitoring the systemic oxidative stress status in post-stroke patients in order to plan a tailored intervention, considering its relationship with functional recovery. Full article

(This article belongs to the Special Issue Oxidative Stress and Inflammation in Cardiovascular Diseases - 3rd Edition)

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16 pages, 2232 KiB

Open AccessArticle

Albumin Redox Modifications Promote Cell Calcification Reflecting the Impact of Oxidative Status on Aortic Valve Disease and Atherosclerosis

by Tamara Sastre-Oliva, Nerea Corbacho-Alonso, Elena Rodriguez-Sanchez, Elisa Mercado-García, Ines Perales-Sanchez, German Hernandez-Fernandez, Cristina Juarez-Alia, Teresa Tejerina, Luis F. López-Almodóvar, Luis R. Padial, Pedro L. Sánchez, Ernesto Martín-Núñez, Natalia López-Andrés, Gema Ruiz-Hurtado, Laura Mourino-Alvarez and Maria G. Barderas

Antioxidants 2024, 13(1), 108; https://doi.org/10.3390/antiox13010108 - 16 Jan 2024

Cited by 2 | Viewed by 1901

Abstract

Calcific aortic valve disease (CAVD) and coronary artery disease (CAD) are related cardiovascular diseases in which common mechanisms lead to tissue calcification. Oxidative stress plays a key role in these diseases and there is also evidence that the redox state of serum albumin exerts a significant influence on these conditions. To further explore this issue, we used multimarker scores (OxyScore and AntioxyScore) to assess the global oxidative status in patients with CAVD, with and without CAD, also evaluating their plasma thiol levels. In addition, valvular interstitial cells were treated with reduced, oxidized, and native albumin to study how this protein and its modifications affect cell calcification. The differences we found suggest that oxidative status is distinct in CAVD and CAD, with differences in redox markers and thiol levels. Importantly, the in vitro interstitial cell model revealed that modified albumin affects cell calcification, accelerating this process. Hence, we show here the importance of the redox system in the development of CAVD, emphasizing the relevance of multimarker scores, while also offering evidence of how the redox state of albumin influences vascular calcification. These data highlight the relevance of understanding the overall redox processes involved in these diseases, opening the door to new studies on antioxidants as potential therapies for these patients. Full article

(This article belongs to the Special Issue Oxidative Stress and Inflammation in Cardiovascular Diseases - 3rd Edition)

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14 pages, 4306 KiB

Open AccessArticle

Differential Effects of High Fat Diets on Resilience to H₂O₂-Induced Cell Death in Mouse Cerebral Arteries: Role for Processed Carbohydrates

by Charles E. Norton, Rebecca L. Shaw and Steven S. Segal

Antioxidants 2023, 12(7), 1433; https://doi.org/10.3390/antiox12071433 - 16 Jul 2023

Cited by 4 | Viewed by 1309

Abstract

High fat, western-style diets increase vascular oxidative stress. We hypothesized that smooth muscle cells and endothelial cells adapt during the consumption of high fat diets to become more resilient to acute oxidative stress. Male C57Bl/6J mice were fed a western-style diet high in fat and processed carbohydrates (WD), a high fat diet that induces obesity (DIO), or their respective control (CD) and standard (SD) diets for 16 weeks. Posterior cerebral arteries (PCAs) were isolated and pressurized for study. During acute exposure to H₂O₂ (200 µM), smooth muscle cell and endothelial cell death were reduced in PCAs from WD, but not DIO mice. WD selectively attenuated mitochondrial membrane potential depolarization and vessel wall Ca²⁺ influx during H₂O₂ exposure. Selective inhibition of transient receptor potential (TRP) V4 or TRPC3 channels reduced smooth muscle cell and endothelial cell death in concert with the vessel wall [Ca²⁺]_i response to H₂O₂ for PCAs from CD mice and eliminated differences between CD and WD. Inhibiting Src kinases reduced smooth muscle cell death along with [Ca²⁺]_i response to H₂O₂ only in PCAs from CD mice and eliminated differences between diets. However, Src kinase inhibition did not alter endothelial cell death. These findings indicate that consuming a WD, but not high fat alone, leads to adaptations that limit Ca²⁺ influx and vascular cell death during exposure to acute oxidative stress. Full article

(This article belongs to the Special Issue Oxidative Stress and Inflammation in Cardiovascular Diseases - 3rd Edition)

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13 pages, 1618 KiB

Open AccessArticle

N-acetylcysteine Amide AD4/NACA and Thioredoxin Mimetic Peptides Inhibit Platelet Aggregation and Protect against Oxidative Stress

by Sonia Eligini, Marco Munno, Daphne Atlas and Cristina Banfi

Antioxidants 2023, 12(7), 1395; https://doi.org/10.3390/antiox12071395 - 7 Jul 2023

Cited by 5 | Viewed by 1647

Abstract

In the present study, we tested the effect of small-molecular-weight redox molecules on collagen-induced platelet aggregation. We used N-acetylcysteine amide (AD4/NACA), the amide form of N-acetylcysteine (NAC), a thiol antioxidant with improved lipophilicity and bioavailability compared to NAC, and the thioredoxin-mimetic (TXM) peptides, TXM-CB3, TXM-CB13, and TXM-CB30. All compounds significantly inhibited platelet aggregation induced by collagen, with TXM-peptides and AD4 being more effective than NAC. The levels of TxB₂ and 12-HETE, the main metabolites derived from the cyclooxygenase and lipoxygenase pathways following platelet activation, were significantly reduced in the presence of AD4, TXM peptides, or NAC, when tested at the highest concentration (0.6 mM). The effects of AD4, TXM-peptides, and NAC were also tested on the clotting time (CT) of whole blood. TXM-CB3 and TXM-CB30 showed the greatest increase in CT. Furthermore, two representative compounds, TXM-CB3 and NAC, showed an increase in the anti-oxidant free sulfhydryl groups of plasma detected via Ellman’s method, suggesting a contribution of plasma factors to the antiaggregating effects. Our results suggest that these small-molecular-weight redox peptides might become useful for the prevention and/or treatment of oxidative stress conditions associated with platelet activation. Full article

(This article belongs to the Special Issue Oxidative Stress and Inflammation in Cardiovascular Diseases - 3rd Edition)

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13 pages, 3030 KiB

Open AccessArticle

Paclitaxel Protects against Isoproterenol-Induced Damage in Rat Myocardium: Its Heme-Oxygenase Mediated Role in Cardiovascular Research

by Danica Matusovits, Zsolt Murlasits, Krisztina Kupai, Zoltán Baráth, Hsu Lin Kang, Péter Osváth, Miklós Szűcs, Dániel Priksz, Béla Juhász, Zsolt Radák, Tamás Várkonyi, Imre Pavo and Anikó Pósa

Antioxidants 2023, 12(5), 1129; https://doi.org/10.3390/antiox12051129 - 20 May 2023

Cited by 2 | Viewed by 1742

Abstract

(1) Background: In cardiovascular applications, paclitaxel inhibits smooth muscle cell proliferation and migration and significantly reduces the occurrence of restenosis and target lesion revascularization. However, the cellular effects of paclitaxel in the myocardium are not well understood; (2) Methods: Wistar rats were divided into four groups: control (CTRL), isoproterenol (ISO) treated (1 mg/kg) and two groups treated with paclitaxel (PAC), which was administrated (10 mg/kg/day) for 5 days by gavage/per os alone or in combination (ISO + PAC) 3 weeks after ISO treatment. Ventricular tissue was harvested 24 h later for measurements of heme oxygenase (HO-1), reduced glutathione (GSH), oxidized glutathione (GSSG), superoxide dismutase (SOD), NF-κB, TNF-α and myeloperoxidase (MPO); (3) Results: HO-1 protein concentration, HO-1 activity, SOD protein concentration and total glutathione significantly decreased in response to ISO treatment. When PAC was administered in conjunction with ISO, HO-1, SOD concentration and total glutathione were not different from control levels. MPO activity, NF-κB concentration and TNF-α protein concentration were significantly increased in the ISO-only group, while the levels of these molecules were restored when PAC was co-administered; (4) Conclusions: Oral administration of PAC can maintain the expression of important antioxidants, anti-inflammatory molecules, HO-1, SOD and GSH, and suppress the production of TNF-α, MPO and NF-κB, which are involved in myocardial damage. The principal component of this cellular defense seems to be the expression of HO-1. Full article

(This article belongs to the Special Issue Oxidative Stress and Inflammation in Cardiovascular Diseases - 3rd Edition)

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18 pages, 1836 KiB

Open AccessArticle

Oxidative Stress and Cardiovascular Risk Factors: The Coronary Artery Risk Development in Young Adults (CARDIA) Study

by Amir S. Heravi, Di Zhao, Erin D. Michos, Henrique Doria De Vasconcellos, Bharath Ambale-Venkatesh, Donald Lloyd-Jones, Pamela J. Schreiner, Jared P. Reis, James M. Shikany, Cora E. Lewis, Chiadi E. Ndumele, Eliseo Guallar, Pamela Ouyang, Ron C. Hoogeveen, Joao A. C. Lima, Wendy S. Post and Dhananjay Vaidya

Antioxidants 2023, 12(3), 555; https://doi.org/10.3390/antiox12030555 - 23 Feb 2023

Cited by 2 | Viewed by 2123

Abstract

Introduction—Oxidative stress is linked to cardiovascular diseases (CVD) and is suggested to vary by sex. However, few population-level studies have explored these associations and the majority comprise populations with advanced CVD. We assessed urinary isoprostane concentrations, a standard measure of oxidative stress, in a relatively young and healthy cohort, hypothesizing that higher oxidative stress is associated with an adverse cardiometabolic profile and female sex. Methods—Oxidative stress was measured in 475 women and 266 men, aged 48–55 years, from the Coronary Artery Risk Development in Young Adults (CARDIA) study using urinary 8-isoprostane (IsoP) and 2,3-dinor-8-isoprostane (IsoP-M). Multivariable-adjusted regression was used to evaluate cross-sectional associations. As secondary analysis, previously measured plasma F2-isoprostanes (plasma IsoP) from another CARDIA subset was similarly analyzed. Results—Mean (SD) ages for men and women were 52.1(2.3) and 52.2(2.2) years, respectively (p = 0.46), and 39% of the participants self-identified as Black (vs. White). Before adjustments, female sex was associated with higher median urinary IsoP (880 vs. 704 ng/g creatinine in men; p < 0.01) and IsoP m (1675 vs. 1284 ng/g creatinine in men; p < 0.01). Higher body mass index (BMI), high-density cholesterol (HDL-C), and triglycerides, current smoking, and less physical activity were associated with higher oxidative stress. Diabetes was not associated with urinary IsoP but was associated with lower IsoP m and plasma IsoP. Higher serum creatinine showed diverging associations with higher plasma and lower urinary isoprostane concentrations. Conclusions—Different isoprostane entities exhibit varying association patterns with CVD risk factors, and therefore are complementary, rather than interchangeable, in assessment of oxidative stress. Still, consistently higher isoprostanes among women, smokers, less active persons, and those with higher BMI and plasma triglycerides could reflect higher oxidative stress among these groups. While urinary isoprostanes are indexed to urinary creatinine due to variations in concentration, caution should be exercised when comparing groups with differing serum creatinine. Full article

(This article belongs to the Special Issue Oxidative Stress and Inflammation in Cardiovascular Diseases - 3rd Edition)

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13 pages, 2009 KiB

Open AccessArticle

Plasma Copper Concentration Is Associated with Cardiovascular Mortality in Male Kidney Transplant Recipients

by Manuela Yepes-Calderón, Daan Kremer, Adrian Post, Camilo G. Sotomayor, Ulrike Seidel, Patricia Huebbe, Tim J. Knobbe, Kai Lüersen, Michele F. Eisenga, Eva Corpeleijn, Martin H. De Borst, Gerjan J. Navis, Gerald Rimbach and Stephan J. L. Bakker

Antioxidants 2023, 12(2), 454; https://doi.org/10.3390/antiox12020454 - 10 Feb 2023

Cited by 3 | Viewed by 1731

Abstract

Kidney transplant recipients (KTR) are at increased risk of cardiovascular mortality. We investigated whether, in KTR, post-transplantation copper status is associated with the risk of cardiovascular mortality and potential effect modification by sex. In this cohort study, plasma copper was measured using mass spectrometry in extensively-phenotyped KTR with a functioning allograft >1-year. Cox regression analyses with the inclusion of multiplicative interaction terms were performed. In 660 KTR (53 ± 13 years old, 56% male), the median baseline plasma copper was 15.42 (IQR 13.53–17.63) µmol/L. During a median follow-up of 5 years, 141 KTR died, 53 (38%) due to cardiovascular causes. Higher plasma copper was associated with an increased risk of cardiovascular mortality in the overall KTR population (HR 1.37; 95% CI, 1.07–1.77 per 1-SD, p = 0.01). Sex was a significant effect modifier of this association (P_interaction = 0.01). Among male KTR, higher plasma copper concentration was independently associated with a two-fold higher risk of cardiovascular mortality (HR 2.09; 95% CI, 1.42–3.07 per 1-SD, p < 0.001). Among female KTR, this association was absent. This evidence offers a rationale for considering a sex-specific assessment of copper’s role in cardiovascular risk evaluation. Further studies are warranted to elucidate whether copper-targeted interventions may decrease cardiovascular mortality in male KTR. Full article

(This article belongs to the Special Issue Oxidative Stress and Inflammation in Cardiovascular Diseases - 3rd Edition)

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13 pages, 1460 KiB

Open AccessArticle

Correlation between Blunted Nocturnal Decrease in Diastolic Blood Pressure and Oxidative Stress: An Observational Study

by Nestor Vazquez-Agra, Anton Cruces-Sande, Estefania Mendez-Alvarez, Ramon Soto-Otero, Sergio Cinza-Sanjurjo, Jose-Enrique Lopez-Paz, Antonio Pose-Reino and Alvaro Hermida-Ameijeiras

Antioxidants 2022, 11(12), 2430; https://doi.org/10.3390/antiox11122430 - 9 Dec 2022

Cited by 3 | Viewed by 1923

Abstract

An impaired nocturnal decrease in diastolic blood pressure (DBP) increases the blood pressure (BP) load, which is a main factor in endothelial dysfunction, atherosclerosis, and arterial stiffness. We aimed to quantify some markers of oxidative stress in hypertensive patients, to compare their levels between individuals with dipper and non-dipper DBP profiles, and to assess their correlation with the nocturnal DBP (nDBP) dipping. It was an observational study that included patients older than 18 years with a diagnosis of essential hypertension who consented to participate. The collected variables were some indices of 24-h ambulatory blood pressure monitoring, demographic, epidemiological, clinical, and laboratory variables. Plasma thiobarbituric acid reactive substances (TBARS) and reduced thiols, together with serum vitamin E, vitamin A, copper (Cu), and zinc (Zn) levels were assessed as oxidative stress markers. We recruited 248 patients with a median age of 56 years (56% women). The percentage of nDBP dipping showed a weak positive correlation with reduced thiol, vitamin E, and vitamin A levels; and a weak negative correlation with Cu levels. We also found a negative correlation between nDBP dipping and the TBARS/Thiol, TBARS/Vitamin E, and TBARS/Vitamin A ratios. After multivariate analysis, we found that increased TBARS/Thiol ratio and serum Cu levels were associated with a higher risk of a non-dipper DBP profile. As in other situations of increased cardiovascular risk, an impaired nDBP decrease may coincide with abnormalities in redox status. Full article

(This article belongs to the Special Issue Oxidative Stress and Inflammation in Cardiovascular Diseases - 3rd Edition)

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