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Role of Oxidative Stress in Cardiac Remodeling and Heart Failure

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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 (31 October 2022) | Viewed by 10532

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Special Issue Editor

Dr. Marina Politi Okoshi

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Guest Editor

Department of Internal Medicine, Botucatu Medical School, Sao Paulo State University, UNESP, Botucatu 18618-687, SP, Brazil
Interests: heart failure; skeletal muscle; cardiac remodeling; physical exercise; cell signaling; ventricular function
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Cardiac remodeling is defined as molecular, cellular, and interstitial cardiac changes that manifest clinically as changes in the size, shape, and function of the heart. Cardiac failure is the final pathway of many cardiac diseases and presents a major public health issue due to its poor prognosis and high prevalence, morbidity, and mortality. Oxidative stress is characterized by an increased ratio between oxygen radical production and scavenging capacity. Although at low levels reactive oxygen species play a role in intracellular signaling pathways, at higher levels they may induce cellular injury, dysfunction, and death. Clinical and experimental studies have shown that oxidative stress is increased in the myocardium and at a systemic level during heart failure, and in the myocardium, increased oxidative stress may result from injured myocytes and may induce additional lesions to myocardial cells, therefore forming a vicious cycle. Despite extensive studies, the molecular pathways involved in heart failure-associated oxidative stress are still not completely understood.

This Special Issue is dedicated to reviews and original research regarding in vitro, animal experiments, and clinical studies about the mechanisms underlying the role of increased oxidative stress in cardiac remodeling and heart failure pathophysiology, clinical manifestations, novel targets, and pharmacological and non-pharmacological treatment.

Dr. Marina Politi Okoshi
Guest Editor

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Keywords

oxidative stress
cardiac failure
signaling pathways
remodeling
left ventricular dysfunction

Published Papers (6 papers)

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Research

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15 pages, 2118 KiB

Open AccessArticle

Effects of Resistance Exercise on Slow-Twitch Soleus Muscle of Infarcted Rats

by Lidiane Moreira Souza, Mariana Janini Gomes, Bruna Brasil Brandao, Luana Urbano Pagan, Mariana Gatto, Felipe Cesar Damatto, Eder Anderson Rodrigues, Thierres Hernani Dias Pontes, Patricia Aparecida Borim, Ana Angelica Henrique Fernandes, Gilson Masahiro Murata, Leonardo Antonio Mamede Zornoff, Paula Schmidt Azevedo, Katashi Okoshi and Marina Politi Okoshi

Antioxidants 2023, 12(2), 291; https://doi.org/10.3390/antiox12020291 - 27 Jan 2023

Cited by 3 | Viewed by 1800

Abstract

Although current guidelines recommend resistance exercise in combination with aerobic training to increase muscle strength and prevent skeletal muscle loss during cardiac remodeling, its effects are not clear. In this study, we evaluated the effects of resistance training on cardiac remodeling and the soleus muscle in long-term myocardial infarction (MI) rats. Methods: Three months after MI induction, male Wistar rats were assigned to Sham (n = 14), MI (n = 9), and resistance exercised MI (R-MI, n = 13) groups. The rats trained three times a week for 12 weeks on a climbing ladder. An echocardiogram was performed before and after training. Protein expression of the insulin-like growth factor (IGF)-1/protein kinase B (Akt)/rapamycin target complex (mTOR) pathway was analyzed by Western blot. Results: Mortality rate was higher in MI than Sham; in the R-MI group, mortality rate was between that in MI and Sham and did not differ significantly from either group. Exercise increased maximal load capacity without changing cardiac structure and left ventricular function in infarcted rats. Infarction size did not differ between infarcted groups. Catalase activity was lower in MI than Sham and glutathione peroxidase lower in MI than Sham and R-MI. Protein expression of p70S6K was lower in MI than Sham and p-FoxO3 was lower in MI than Sham and R-MI. Energy metabolism did not differ between groups, except for higher phosphofrutokinase activity in R-MI than MI. Conclusion: Resistance exercise is safe and increases muscle strength regardless structural and functional cardiac changes in myocardial-infarcted rats. This exercise modality attenuates soleus glycolytic metabolism changes and improves the expression of proteins required for protein turnover and antioxidant response. Full article

(This article belongs to the Special Issue Role of Oxidative Stress in Cardiac Remodeling and Heart Failure)

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14 pages, 649 KiB

Open AccessArticle

Circulating Reactive Oxygen Species in Adults with Congenital Heart Disease

by Inne Vanreusel, Dorien Vermeulen, Inge Goovaerts, Tibor Stoop, Bert Ectors, Jacky Cornelis, Wendy Hens, Erwin de Bliek, Hilde Heuten, Emeline M. Van Craenenbroeck, An Van Berendoncks, Vincent F. M. Segers and Jacob J. Briedé

Antioxidants 2022, 11(12), 2369; https://doi.org/10.3390/antiox11122369 - 30 Nov 2022

Cited by 5 | Viewed by 1370

Abstract

Oxidative stress is an important pathophysiological mechanism in the development of numerous cardiovascular disorders, but few studies have examined the levels of oxidative stress in adults with congenital heart disease (CHD). The objective of this study was to investigate oxidative stress levels in adults with CHD and the association with inflammation, exercise capacity and endothelial function. To this end, 36 adults with different types of CHD and 36 age- and gender-matched healthy controls were enrolled. Blood cell counts, hs-CRP, NT-proBNP, fasting glucose, cholesterol levels, iron saturation and folic acid concentrations were determined in venous blood samples. Levels of superoxide anion radical in whole blood were determined using electron paramagnetic resonance spectroscopy in combination with the spin probe CMH. Physical activity was assessed with the IPAQ-SF questionnaire. Vascular function assessment (EndoPAT) and cardiopulmonary exercise testing were performed in the patient group. Superoxide anion radical levels were not statistically significantly different between adults with CHD and the matched controls. Moreover, oxidative stress did not correlate with inflammation, or with endothelial function or cardiorespiratory fitness in CHD; however, a significant negative correlation with iron saturation was observed. Overall, whole blood superoxide anion radical levels in adults with CHD were not elevated, but iron levels seem to play a more important role in oxidative stress mechanisms in CHD than in healthy controls. More research will be needed to improve our understanding of the underlying pathophysiology of CHD. Full article

(This article belongs to the Special Issue Role of Oxidative Stress in Cardiac Remodeling and Heart Failure)

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11 pages, 1996 KiB

Open AccessArticle

Maintenance over Time of the Effect Produced by Esmolol on the Structure and Function of Coronary Arteries in Hypertensive Heart Diseases

by Raquel Martín-Oropesa, Pilar Rodríguez-Rodríguez, Laia Pazó-Sayós, Ana Arnalich-Montiel, Silvia Magdalena Arribas, Maria Carmen González and Begoña Quintana-Villamandos

Antioxidants 2022, 11(10), 2042; https://doi.org/10.3390/antiox11102042 - 17 Oct 2022

Viewed by 1272

Abstract

We previously observed that esmolol treatment for 48 h reduced vascular lesions in spontaneously hypertensive rats (SHRs). Therefore, we investigated whether this beneficial effect is persistent after withdrawal. Fourteen-month-old SHRs (SHR-Es) were treated with esmolol (300 μg/kg/min) or a vehicle for 48 h. Two separate groups were also given identical treatment, but they were then monitored for a further 1 week and 1 month after drug withdrawal. We analyzed the geometry and composition of the coronary artery, vascular reactivity and plasma redox status. Esmolol significantly decreased wall thickness (medial layer thickness and cell count), external diameter and cross-sectional area of the artery, and this effect persisted 1 month after drug withdrawal. Esmolol significantly improved endothelium-dependent relaxation by ACh (10⁻⁹–10⁻⁴ mol/L); this effect persisted 1 week (10⁻⁹–10⁻⁴ mol/L) and 1 month (10⁻⁶–10⁻⁴ mol/L) after withdrawal. Esmolol reduced the contraction induced by 5-HT (3 × 10⁻⁸–3 × 10⁻⁵ mol/L), and this effect persisted 1 week after withdrawal (10⁻⁶–3 × 10⁻⁵ mol/L). Esmolol increased nitrates and reduced glutathione, and it decreased malondialdehyde and carbonyls; this enhancement was maintained 1 month after withdrawal. This study shows that the effect of esmolol on coronary remodeling is persistent after treatment withdrawal in SHRs, and the improvement in plasma oxidative status can be implicated in this effect. Full article

(This article belongs to the Special Issue Role of Oxidative Stress in Cardiac Remodeling and Heart Failure)

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16 pages, 4100 KiB

Open AccessArticle

Mitochondrial Oxidative Stress Promotes Cardiac Remodeling in Myocardial Infarction through the Activation of Endoplasmic Reticulum Stress

by Francisco V. Souza-Neto, Fabian Islas, Sara Jiménez-González, María Luaces, Bunty Ramchandani, Ana Romero-Miranda, Beatriz Delgado-Valero, Elena Roldan-Molina, Melchor Saiz-Pardo, Mª Ángeles Cerón-Nieto, Luis Ortega-Medina, Ernesto Martínez-Martínez and Victoria Cachofeiro

Antioxidants 2022, 11(7), 1232; https://doi.org/10.3390/antiox11071232 - 23 Jun 2022

Cited by 5 | Viewed by 2297

Abstract

We have evaluated cardiac function and fibrosis in infarcted male Wistar rats treated with MitoQ (50 mg/kg/day) or vehicle for 4 weeks. A cohort of patients admitted with a first episode of acute MI were also analyzed with cardiac magnetic resonance and T1 mapping during admission and at a 12-month follow-up. Infarcted animals presented cardiac hypertrophy and a reduction in the left ventricular ejection fraction (LVEF) and E- and A-waves (E/A) ratio when compared to controls. Myocardial infarction (MI) rats also showed cardiac fibrosis and endoplasmic reticulum (ER) stress activation. Binding immunoglobulin protein (BiP) levels, a marker of ER stress, were correlated with collagen I levels. MitoQ reduced oxidative stress and prevented all these changes without affecting the infarct size. The LVEF and E/A ratio in patients with MI were 57.6 ± 7.9% and 0.96 ± 0.34, respectively. No major changes in cardiac function, extracellular volume fraction (ECV), or LV mass were observed at follow-up. Interestingly, the myeloperoxidase (MPO) levels were associated with the ECV in basal conditions. BiP staining and collagen content were also higher in cardiac samples from autopsies of patients who had suffered an MI than in those who had died from other causes. These results show the interactions between mitochondrial oxidative stress and ER stress, which can result in the development of diffuse fibrosis in the context of MI. Full article

(This article belongs to the Special Issue Role of Oxidative Stress in Cardiac Remodeling and Heart Failure)

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Review

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11 pages, 544 KiB

Open AccessReview

Oxidative Stress as a Therapeutic Target of Cardiac Remodeling

by Danilo Martins, Leonardo Rufino Garcia, Diego Aparecido Rios Queiroz, Taline Lazzarin, Carolina Rodrigues Tonon, Paola da Silva Balin, Bertha Furlan Polegato, Sergio Alberto Rupp de Paiva, Paula Schmidt Azevedo, Marcos Ferreira Minicucci and Leonardo Zornoff

Antioxidants 2022, 11(12), 2371; https://doi.org/10.3390/antiox11122371 - 30 Nov 2022

Cited by 10 | Viewed by 1609

Abstract

Cardiac remodeling is defined as a group of molecular, cellular, and interstitial changes that clinically manifest as changes in the heart’s size, mass, geometry, and function after different stimuli. It is important to emphasize that remodeling plays a pathophysiological role in the onset and progression of ventricular dysfunction and subsequent heart failure. Therefore, strategies to mitigate this process are critical. Different factors, including neurohormonal activation, can regulate the remodeling process and increase cell death, alterations in contractile and regulatory proteins, alterations in energy metabolism, changes in genomics, inflammation, changes in calcium transit, metalloproteases activation, fibrosis, alterations in matricellular proteins, and changes in left ventricular geometry, among other mechanisms. More recently, the role of reactive oxygen species and oxidative stress as modulators of remodeling has been gaining attention. Therefore, this review assesses the role of oxidative stress as a therapeutic target of cardiac remodeling. Full article

(This article belongs to the Special Issue Role of Oxidative Stress in Cardiac Remodeling and Heart Failure)

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16 pages, 656 KiB

Open AccessReview

Role of Nutrients and Foods in Attenuation of Cardiac Remodeling through Oxidative Stress Pathways

by Taline Lazzarin, Leonardo Rufino Garcia, Danilo Martins, Diego Aparecido Rios Queiroz, Carolina Rodrigues Tonon, Paola da Silva Balin, Bertha Furlan Polegato, Sergio Alberto Rupp de Paiva, Paula Schmidt Azevedo, Marcos Minicucci and Leonardo Zornoff

Antioxidants 2022, 11(10), 2064; https://doi.org/10.3390/antiox11102064 - 20 Oct 2022

Cited by 4 | Viewed by 1642

Abstract

Cardiac remodeling is defined as a group of molecular, cellular, and interstitial changes that manifest clinically as changes in the heart’s size, mass, geometry, and function after different injuries. Importantly, remodeling is associated with increased risk of ventricular dysfunction and heart failure. Therefore, strategies to attenuate this process are critical. Reactive oxygen species and oxidative stress play critical roles in remodeling. Importantly, antioxidative dietary compounds potentially have protective properties against remodeling. Therefore, this review evaluates the role of nutrients and food as modulators of cardiac remodeling. Full article

(This article belongs to the Special Issue Role of Oxidative Stress in Cardiac Remodeling and Heart Failure)

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