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Antioxidants
Special Issues
Oxidative Balance and Heart Function: A Physiological Lifelong Challenge
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Oxidative Balance and Heart Function: A Physiological Lifelong Challenge

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 (30 June 2023) | Viewed by 9635

Special Issue Editors

Prof. Dr. Simone Guarnieri

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Guest Editor
Department of Neuroscience, Imaging and Clinical Sciences, Center for Advanced Studies and Technology (CAST), University “G. d’Annunzio” Chieti-Pescara, Via dei Vestini, 31, 66100 Chieti, Italy
Interests: ROS; Calcium; live imaging; cardiac muscle; skeletal muscle
Dr. Caterina Morabito

E-Mail Website
Guest Editor
Department of Neuroscience, Imaging and Clinical Sciences and Center for Advanced Studies and Technology (CAST), “G. d’Annunzio” University of Chieti-Pescara, 66100 Chieti, Italy
Interests: simulated-microgravity; lymphocytes; oxidative stress; cytoskeletal remodelling; Cell Shape

Special Issue Information

Dear Colleagues,

Free radicals are highly reactive molecules that play a crucial part in different physiological and
physiopathological processes including cell signaling, inflammation and immune defense. In chemical terms, the actions of free radicals can affect the cell physiological response, increasing or decreasing the levels of unstable products able to react with other molecules or acting as physiological process modulators that cause, if not properly balanced, damage to cellular and sub-cellular components.

From this point of view, free radicals and reactive oxygen species (ROS) can be considered not only as "cell toxic species" but also as cell messengers. Thus, they induce oxidative modification in protein, nucleic acid and lipids, acting as second messengers controlling changes in molecular pathways. Emerging evidence demonstrates that ROS, via post-translational modifications, denoted as ‘oxidative eustress’, has a central role in the heart, at the physiological level.

At the physiological nanomolar level, ROS are mediators of signaling through specific protein targets,
which are involved in metabolic regulation to support cardiomyocytes function and adaptation. On the other hand, an excess of ROS is detrimental for cardiac function. In this scenario, the redox balancing in the heart is a direct consequence of ROS and ROS countermeasures, acting together to maintain homeostasis. Alteration of this equilibrium could contribute to the physiological aging of the heart and to the onset of pathological conditions. In addition, the degree of these alterations could be also a consequence of a suboptimal lifestyle or environmental challenges that cause metabolism to be more prone to ROS.

The aim of this Special Issue is to focus on the most recent discoveries on ROS-induced cell
responses influencing cardiac function, and to highlight the different molecular mechanisms, signaling pathways and biological strategies by which cardiomyocytes adapt/react to oxidative stress.

Prof. Dr. Simone Guarnieri
Dr. Caterina Morabito
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

  • antioxidant
  • oxidative stress
  • heart
  • lifestyle
  • environmental challenges
  • reactive oxygen species
  • aging
  • post-translational modifications
  • nutrition
  • cardiomyocites
  • metabolism

Published Papers (4 papers)

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Research

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14 pages, 3304 KiB  
Article
Cytokine Adsorber Use during DCD Heart Perfusion Counteracts Coronary Microvascular Dysfunction
by Lars Saemann, Fabio Hoorn, Adrian-Iustin Georgevici, Sabine Pohl, Sevil Korkmaz-Icöz, Gábor Veres, Yuxing Guo, Matthias Karck, Andreas Simm, Folker Wenzel and Gábor Szabó
Antioxidants 2022, 11(11), 2280; https://doi.org/10.3390/antiox11112280 - 17 Nov 2022
Cited by 2 | Viewed by 1572
Abstract
Microvascular dysfunction (MVD) in cardiac allografts is associated with an impaired endothelial function in the coronary microvasculature. Ischemia/reperfusion injury (IRI) deteriorates endothelial function. Hearts donated after circulatory death (DCD) are exposed to warm ischemia before initiating ex vivo blood perfusion (BP). The impact [...] Read more.
Microvascular dysfunction (MVD) in cardiac allografts is associated with an impaired endothelial function in the coronary microvasculature. Ischemia/reperfusion injury (IRI) deteriorates endothelial function. Hearts donated after circulatory death (DCD) are exposed to warm ischemia before initiating ex vivo blood perfusion (BP). The impact of cytokine adsorption during BP to prevent MVD in DCD hearts is unknown. In a porcine DCD model, we assessed the microvascular function of hearts after BP with (DCD-BPCytoS, n = 5) or without (DCD-BP, n = 5) cytokine adsorption (CytoSorb®). Microvascular autoregulation was assessed by increasing the coronary perfusion pressure, while myocardial microcirculation was measured by Laser-Doppler-Perfusion (LDP). We analyzed the immunoreactivity of arteriolar oxidative stress markers nitrotyrosine and 4-hydroxy-2-nonenal (HNE), endothelial injury indicating cell adhesion molecules CD54, CD106 and CD31, and eNOS. We profiled the concentration of 13 cytokines in the perfusate. The expression of 84 genes was determined and analyzed using machine learning and decision trees. Non-DCD hearts served as a control for the gene expression analysis. Compared to DCD-BP, relative LDP was improved in the DCD-BPCytoS group (1.51 ± 0.17 vs. 1.08 ± 0.17). Several pro- and anti-inflammatory cytokines were reduced in the DCD-BPCytoS group. The expression of eNOS significantly increased, and the expression of nitrotyrosine, HNE, CD54, CD106, and CD31, markers of endothelial injury, majorly decreased in the DCD-BPCytoS group. Three genes allowed exact differentiation between groups; regulation of HIF1A enabled differentiation between perfusion (DCD-BP, DCD-BPCytoS) and non-perfusion groups. CAV1 allowed differentiation between BP and BPCytoS. The use of a cytokine adsorption device during BP counteracts preload-dependent MVD and preserves the microvascular endothelium by preventing oxidative stress and IRI of coronary arterioles of DCD hearts. Full article
(This article belongs to the Special Issue Oxidative Balance and Heart Function: A Physiological Lifelong Challenge)
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14 pages, 4278 KiB  
Article
NADPH Oxidase Mediates Oxidative Stress and Ventricular Remodeling through SIRT3/FOXO3a Pathway in Diabetic Mice
by Jiuchun Qiu, Daiqi Liu, Pengsha Li, Lingling Zhou, Lu Zhou, Xing Liu, Yue Zhang, Meng Yuan, Gary Tse, Guangping Li and Tong Liu
Antioxidants 2022, 11(9), 1745; https://doi.org/10.3390/antiox11091745 - 02 Sep 2022
Cited by 4 | Viewed by 1946
Abstract
Oxidative stress and mitochondrial dysfunction are important mechanisms of ventricular remodeling, predisposed to the development of diabetic cardiomyopathy (DCM) in type 2 diabetes mellitus. In this study, we have successfully established a model of type 2 diabetes using a high-fat diet (HFD) in [...] Read more.
Oxidative stress and mitochondrial dysfunction are important mechanisms of ventricular remodeling, predisposed to the development of diabetic cardiomyopathy (DCM) in type 2 diabetes mellitus. In this study, we have successfully established a model of type 2 diabetes using a high-fat diet (HFD) in combination with streptozotocin (STZ). The mice were divided into three groups of six at random: control, diabetes, and diabetes with apocynin and the H9c2 cell line was used as an in vitro model for investigation. We examined the molecular mechanisms of nicotinamide adenine dinucleotide phosphate (NADPH) oxidase activation on mitochondrial dysfunction and ventricular remodeling in the diabetic mouse model. Hyperglycemia-induced oxidative stress led to a reduced expression of sirtuin 3 (SIRT3), thereby promoting forkhead box class O 3a (FOXO3a) acetylation in ventricular tissue and H9c2 cells. Reactive oxygen species (ROS) overproduction promoted ventricular structural modeling and conduction defects. These alterations were mitigated by inhibiting NADPH oxidase with the pharmaceutical drug apocynin (APO). Apocynin improved SIRT3 and Mn-SOD expression in H9c2 cells transfected with SIRT3 siRNA. In our diabetic mouse model, apocynin improved myocardial mitochondrial function and ROS overproduction through the recovery of the SIRT3/FOXO3a pathway, thereby reducing ventricular remodeling and the incidence of DCM. Full article
(This article belongs to the Special Issue Oxidative Balance and Heart Function: A Physiological Lifelong Challenge)
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Review

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13 pages, 1625 KiB  
Review
Novel Therapeutic Approaches Enhance PGC1-alpha to Reduce Oxidant Stress-Inflammatory Signaling and Improve Functional Recovery in Hibernating Myocardium
by Rishav Aggarwal, Koray N. Potel, Edward O. McFalls, Tammy A. Butterick and Rosemary F. Kelly
Antioxidants 2022, 11(11), 2155; https://doi.org/10.3390/antiox11112155 - 31 Oct 2022
Cited by 6 | Viewed by 2877
Abstract
Ischemic heart disease affects millions of people around the world. Current treatment options, including coronary artery bypass grafting, do not result in full functional recovery, highlighting the need for novel adjunctive therapeutic approaches. Hibernation describes the myocardial response to prolonged ischemia and involves [...] Read more.
Ischemic heart disease affects millions of people around the world. Current treatment options, including coronary artery bypass grafting, do not result in full functional recovery, highlighting the need for novel adjunctive therapeutic approaches. Hibernation describes the myocardial response to prolonged ischemia and involves a set of complex cytoprotective metabolic and functional adaptations. PGC1-alpha, a key regulator of mitochondrial energy metabolism and inhibitor of oxidant-stress-inflammatory signaling, is known to be downregulated in hibernating myocardium. PGC1-alpha is a critical component of cellular stress responses and links cellular metabolism with inflammation in the ischemic heart. While beneficial in the acute setting, a chronic state of hibernation can be associated with self-perpetuating oxidant stress-inflammatory signaling which leads to tissue injury. It is likely that incomplete functional recovery following revascularization of chronically ischemic myocardium is due to persistence of metabolic changes as well as prooxidant and proinflammatory signaling. Enhancement of PGC1-alpha signaling has been proposed as a possible way to improve functional recovery in patients with ischemic heart disease. Adjunctive mesenchymal stem cell therapy has been shown to induce PGC1-alpha signaling in hibernating myocardium and could help improve clinical outcomes for patients undergoing bypass surgery. Full article
(This article belongs to the Special Issue Oxidative Balance and Heart Function: A Physiological Lifelong Challenge)
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18 pages, 1542 KiB  
Review
High Exogenous Antioxidant, Restorative Treatment (Heart) for Prevention of the Six Stages of Heart Failure: The Heart Diet
by Ram B. Singh, Jan Fedacko, Dominik Pella, Ghizal Fatima, Galal Elkilany, Mahmood Moshiri, Krasimira Hristova, Patrik Jakabcin and Natalia Vaňova
Antioxidants 2022, 11(8), 1464; https://doi.org/10.3390/antiox11081464 - 27 Jul 2022
Cited by 7 | Viewed by 2640
Abstract
The exact pathophysiology of heart failure (HF) is not yet known. Western diet, characterized by highly sweetened foods, as well as being rich in fat, fried foods, red meat and processed meat, eggs, and sweet beverages, may cause inflammation, leading to oxidative dysfunction [...] Read more.
The exact pathophysiology of heart failure (HF) is not yet known. Western diet, characterized by highly sweetened foods, as well as being rich in fat, fried foods, red meat and processed meat, eggs, and sweet beverages, may cause inflammation, leading to oxidative dysfunction in the cardiac ultra-structure. Oxidative function of the myocardium and how oxidative dysfunction causes physio-pathological remodeling, leading to HF, is not well known. Antioxidants, such as polyphenolics and flavonoids, omega-3 fatty acids, and other micronutrients that are rich in Indo-Mediterranean-type diets, could be protective in sustaining the oxidative functions of the heart. The cardiomyocytes use glucose and fatty acids for the physiological functions depending upon the metabolic requirements of the heart. Apart from toxicity due to glucose, lipotoxicity also adversely affects the cardiomyocytes, which worsen in the presence of deficiency of endogenous antioxidants and deficiency of exogenous antioxidant nutrients in the diet. The high-sugar-and-high-fat-induced production of ceramide, advanced glycation end products (AGE) and triamino-methyl-N-oxide (TMAO) can predispose individuals to oxidative dysfunction and Ca-overloading. The alteration in the biology may start with normal cardiac cell remodeling to biological remodeling due to inflammation. An increase in the fat content of a diet in combination with inducible nitric oxide synthase (NOSi) via N-arginine methyl ester has been found to preserve the ejection fraction in HF. It is proposed that a greater intake of high exogenous antioxidant restorative treatment (HEART) diet, polyphenolics and flavonoids, as well as cessation of red meat intake and egg, can cause improvement in the oxidative function of the heart, by inhibiting oxidative damage to lipids, proteins and DNA in the cell, resulting in beneficial effects in the early stage of the Six Stages of HF. There is an unmet need to conduct cohort studies and randomized, controlled studies to demonstrate the role of the HEART diet in the treatment of HF. Full article
(This article belongs to the Special Issue Oxidative Balance and Heart Function: A Physiological Lifelong Challenge)
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