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Antioxidants
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NOS/NO System and Heart
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NOS/NO System and Heart

A special issue of Antioxidants (ISSN 2076-3921). This special issue belongs to the section "ROS, RNS and RSS".

Deadline for manuscript submissions: closed (20 October 2021) | Viewed by 15583

Special Issue Editors

Prof. Dr. Maria Carmela Cerra

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Guest Editor
Laboratory of Organ and System Physiology, Department of Biology, Ecology and Earth Sciences, Via Ponte Pietro Bucci Cubo 6c, 87036 Rende, CS, Italy
Interests: adaptive and environmental cardiac physiology: from polar to tropical and temperate fish; humoral control of the vertebrate heart: natriuretic peptides, angiotensin II, chromogranin-a-derived peptides, selenoprotein T, β3-adrenergic receptors; ischemic cardioprotection in mammals: chromogranin-a-derived peptides, selenoprotein T; cardiovascular role of nutrition-related substances
Prof. Sandra Imbrogno

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Guest Editor
Laboratory of Organ and System Physiology, Department of Biology, Ecology and Earth Sciences, Via Ponte Pietro Bucci cubo 6c, 87036 Rende, CS, Italy
Interests: Morpho-functional design of the vertebrate heart; Cardiac hormones, nitric oxide and signalling; Cardiac functional adaptation to humoral (Angiotensin II, Chromogranin-A-derived peptides, Selenoprotein T, β3-adrenergic receptors) and environmental (hypoxia, temperature) stress
Dr. Alfonsina Gattuso

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Guest Editor
Laboratory of Organ and System Physiology, Department of Biology, Ecology and Earth Sciences, University of Calabria, Rende, CS, Italy
Interests: comparative cardiac physiology; heart mechanics; nitric oxide; cardio-active peptides; signal transduction; hypoxia tolerance

Special Issue Information

Dear Colleagues,

More than twenty years have passed since the Nobel Prize in Physiology or Medicine was awarded in 1998 for the discovery of the cardiovascular properties of nitric oxide (NO). Now this gas is definitively recognized as an essential autocrine–paracrine modulatory molecule for the heart. Generated by differently regulated nitric oxide synthase (NOS) isoenzymes, it coordinates many intracardiac pathways under basal conditions and in the presence of physiological and pathological challenges. Once produced, NO is rapidly metabolized to nitrite and nitrate, highly reactive metabolites that, under low oxygen, can be reconverted to NO, giving rise to a rich and fine nitrosative equilibrium, crucial for cardiac modulation.

The importance of the NOS/NO system in heart homeostasis is documented by its long evolutionary history, being present and functional in mammalian and non-mammalian vertebrates and invertebrates. By acting beat-to-beat, as well as in short (e.g., excitation–contraction coupling, responses to endocrines and neurotransmitters) and long (modulation of gene expression, embryonic development) term, it elicits a fine spatiotemporal cardiac modulation and contributes to cardioprotective programs and to the mechanisms of adaptation to stress.

The cardiac properties of the NOS/NO system are still under remarkable research attention not only in a biomedical context, but also on a curiosity-driven base. Of growing interest are studies on the nitrergic system in animal models characterized by a morphofunctional design of the heart that differs from that of mammals, and in species that possess peculiar—and often extreme—traits of cardiac plasticity in response to stress.

We invite you to contribute with your latest research findings or review articles to this Special Issue with the aim to provide an updated framework of information on the NOS/NO system in cardiac homeostasis of invertebrates and vertebrates, from molecules to organs and systems. Contributions on the old evolutionary roots of the cardiac nitrergic control, its importance during heart development and stress adaptation, and on the translational potential of animal studies, would complete the topic.

Prof. Maria Carmela Cerra
Prof. Sandra Imbrogno
Dr. Alfonsina Gattuso
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.

Published Papers (6 papers)

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Research

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17 pages, 2837 KiB  
Article
An ACE2-Alamandine Axis Modulates the Cardiac Performance of the Goldfish Carassius auratus via the NOS/NO System
by Mariacristina Filice, Rosa Mazza, Sandra Imbrogno, Olga Mileti, Noemi Baldino, Amilcare Barca, Gianmarco Del Vecchio, Tiziano Verri, Alfonsina Gattuso and Maria Carmela Cerra
Antioxidants 2022, 11(4), 764; https://doi.org/10.3390/antiox11040764 - 12 Apr 2022
Cited by 2 | Viewed by 1629
Abstract
Alamandine is a peptide of the Renin Angiotensin System (RAS), either generated from Angiotensin A via the Angiotensin Converting Enzyme 2 (ACE2), or directly from Ang-(1–7). In mammals, it elicits cardioprotection via Mas-related G-protein-coupled receptor D (MrgD), and the NOS/NO system. In teleost [...] Read more.
Alamandine is a peptide of the Renin Angiotensin System (RAS), either generated from Angiotensin A via the Angiotensin Converting Enzyme 2 (ACE2), or directly from Ang-(1–7). In mammals, it elicits cardioprotection via Mas-related G-protein-coupled receptor D (MrgD), and the NOS/NO system. In teleost fish, RAS is known to modulate heart performance. However, no information is available on the presence of a cardioactive ACE2/Alamandine axis. To fill this gap, we used the cyprinid teleost Carassius auratus (goldfish) for in silico and in vitro analyses. Via the NCBI Blast P suite we found that in cyprinids ace2 is phylogenetically detectable in a subcluster of proteins including ace2-like isoforms, and is correlated with a hypoxia-dependent pathway. By real-time PCR, Western Blotting, and HPLC, ACE2 and Alamandine were identified in goldfish heart and plasma, respectively. Both increased after chronic exposure to low O2 (2.6 mg O2 L−1). By using an ex-vivo working goldfish-heart preparation, we observed that in vitro administration of exogenous Alamandine dose-dependently stimulates myocardial contractility starting from 10−11 M. The effect that involved Mas-related receptors and PKA occurred via the NOS/NO system. This was shown by exposing the perfused heart to the NOS inhibitor L-NMMA (10−5 M) that abolished the cardiac effect of Alamandine and was supported by the increased expression of the phosphorylated NOS enzyme in the extract from goldfish heart exposed to 10−10 M Alamandine. Our data are the first to show that an ACE2/Alamandine axis is present in the goldfish C. auratus and, to elicit cardiac modulation, requires the obligatory involvement of the NOS/NO system. Full article
(This article belongs to the Special Issue NOS/NO System and Heart)
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15 pages, 17874 KiB  
Article
HNO Protects the Myocardium against Reperfusion Injury, Inhibiting the mPTP Opening via PKCε Activation
by Daniele Mancardi, Pasquale Pagliaro, Lisa A. Ridnour, Carlo G. Tocchetti, Katrina Miranda, Magdalena Juhaszova, Steven J. Sollott, David A. Wink and Nazareno Paolocci
Antioxidants 2022, 11(2), 382; https://doi.org/10.3390/antiox11020382 - 14 Feb 2022
Cited by 10 | Viewed by 1895
Abstract
Donors of nitroxyl (HNO), the one electron-reduction product of nitric oxide (NO.), positively modulate cardiac contractility/relaxation while limiting ischemia-reperfusion (I/R) injury. The mechanisms underpinning HNO anti-ischemic effects remain poorly understood. Using isolated perfused rat hearts subjected to 30 min global ischemia/1 [...] Read more.
Donors of nitroxyl (HNO), the one electron-reduction product of nitric oxide (NO.), positively modulate cardiac contractility/relaxation while limiting ischemia-reperfusion (I/R) injury. The mechanisms underpinning HNO anti-ischemic effects remain poorly understood. Using isolated perfused rat hearts subjected to 30 min global ischemia/1 or 2 h reperfusion, here we tested whether, in analogy to NO., HNO protection requires PKCε translocation to mitochondria and KATP channels activation. To this end, we compared the benefits afforded by ischemic preconditioning (IPC; 3 cycles of I/R) with those eventually granted by the NO. donor, diethylamine/NO, DEA/NO, and two chemically unrelated HNO donors: Angeli’s salt (AS, a prototypic donor) and isopropylamine/NO (IPA/NO, a new HNO releaser). All donors were given for 19 min before I/R injury. In control I/R hearts (1 h reperfusion), infarct size (IS) measured via tetrazolium salt staining was 66 ± 5.5% of the area at risk. Both AS and IPA/NO were as effective as IPC in reducing IS [30.7 ± 2.2 (AS), 31 ± 2.9 (IPA/NO), and 31 ± 0.8 (IPC), respectively)], whereas DEA/NO was significantly less so (36.2 ± 2.6%, p < 0.001 vs. AS, IPA/NO, or IPC). IPA/NO protection was still present after 120 min of reperfusion, and the co-infusion with the PKCε inhibitor (PKCV1-2500 nM) prevented it (IS = 30 ± 0.5 vs. 61 ± 1.8% with IPA/NO alone, p < 0.01). Irrespective of the donor, HNO anti-ischemic effects were insensitive to the KATP channel inhibitor, 5-OH decanoate (5HD, 100 μM), that, in contrast, abrogated DEA/NO protection. Finally, both HNO donors markedly enhanced the mitochondrial permeability transition pore (mPTP) ROS threshold over control levels (≅35–40%), an action again insensitive to 5HD. Our study shows that HNO donors inhibit mPTP opening, thus limiting myocyte loss at reperfusion, a beneficial effect that requires PKCε translocation to the mitochondria but not mitochondrial K+ channels activation. Full article
(This article belongs to the Special Issue NOS/NO System and Heart)
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13 pages, 4506 KiB  
Article
Effects of Remote Ischaemic Preconditioning on the Internal Thoracic Artery Nitric Oxide Synthase Isoforms in Patients Undergoing Coronary Artery Bypass Grafting
by Aleksandra Jankovic, Tamara Zakic, Miroslav Milicic, Dragana Unic-Stojanovic, Andjelika Kalezic, Aleksandra Korac, Miomir Jovic and Bato Korac
Antioxidants 2021, 10(12), 1910; https://doi.org/10.3390/antiox10121910 - 29 Nov 2021
Cited by 2 | Viewed by 1730
Abstract
Remote ischaemic preconditioning (RIPC) is a medical procedure that consists of repeated brief periods of transient ischaemia and reperfusion of distant organs (limbs) with the ability to provide internal organ protection from ischaemia. Even though RIPC has been successfully applied in patients with [...] Read more.
Remote ischaemic preconditioning (RIPC) is a medical procedure that consists of repeated brief periods of transient ischaemia and reperfusion of distant organs (limbs) with the ability to provide internal organ protection from ischaemia. Even though RIPC has been successfully applied in patients with myocardial infarction during coronary revascularization (surgery/percutaneous angioplasty), the underlying molecular mechanisms are yet to be clarified. Thus, our study aimed to determine the role of nitric oxide synthase (NOS) isoforms in RIPC-induced protection (3 × 5 min of forearm ischaemia with 5 min of reperfusion) of arterial graft in patients undergoing urgent coronary artery bypass grafting (CABG). We examined RIPC effects on specific expression and immunolocalization of three NOS isoforms — endothelial (eNOS), inducible (iNOS) and neuronal (nNOS) in patients’ internal thoracic artery (ITA) used as a graft. We found that the application of RIPC protocol leads to an increased protein expression of eNOS, which was further confirmed with strong eNOS immunopositivity, especially in the endothelium and smooth muscle cells of ITA. The same analysis of two other NOS isoforms, iNOS and nNOS, showed no significant differences between patients undergoing CABG with or without RIPC. Our results demonstrate RIPC-induced upregulation of eNOS in human ITA, pointing to its significance in achieving protective phenotype on a systemic level with important implications for graft patency. Full article
(This article belongs to the Special Issue NOS/NO System and Heart)
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18 pages, 1542 KiB  
Article
The Relationship between Myoglobin, Aerobic Capacity, Nitric Oxide Synthase Activity and Mitochondrial Function in Fish Hearts
by Lucie Gerber, Kathy A. Clow, William R. Driedzic and Anthony K. Gamperl
Antioxidants 2021, 10(7), 1072; https://doi.org/10.3390/antiox10071072 - 3 Jul 2021
Cited by 1 | Viewed by 3099
Abstract
The dynamic interactions between nitric oxide (NO) and myoglobin (Mb) in the cardiovascular system have received considerable attention. The loss of Mb, the principal O2 carrier and a NO scavenger/producer, in the heart of some red-blooded fishes provides a unique opportunity for [...] Read more.
The dynamic interactions between nitric oxide (NO) and myoglobin (Mb) in the cardiovascular system have received considerable attention. The loss of Mb, the principal O2 carrier and a NO scavenger/producer, in the heart of some red-blooded fishes provides a unique opportunity for assessing this globin’s role in NO homeostasis and mitochondrial function. We measured Mb content, activities of enzymes of NO and aerobic metabolism [NO Synthase (NOS) and citrate synthase, respectively] and mitochondrial parameters [Complex-I and -I+II respiration, coupling efficiency, reactive oxygen species production/release rates and mitochondrial sensitivity to inhibition by NO (i.e., NO IC50)] in the heart of three species of red-blooded fish. The expression of Mb correlated positively with NOS activity and NO IC50, with low NOS activity and a reduced NO IC50 in the Mb-lacking lumpfish (Cyclopterus lumpus) as compared to the Mb-expressing Atlantic salmon (Salmo salar) and short-horned sculpin (Myoxocephalus scorpius). Collectively, our data show that NO levels are fine-tuned so that NO homeostasis and mitochondrial function are preserved; indicate that compensatory mechanisms are in place to tightly regulate [NO] and mitochondrial function in a species without Mb; and strongly suggest that the NO IC50 for oxidative phosphorylation is closely related to a fish’s hypoxia tolerance. Full article
(This article belongs to the Special Issue NOS/NO System and Heart)
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Review

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19 pages, 813 KiB  
Review
Hypoxic and Thermal Stress: Many Ways Leading to the NOS/NO System in the Fish Heart
by Mariacristina Filice, Sandra Imbrogno, Alfonsina Gattuso and Maria Carmela Cerra
Antioxidants 2021, 10(9), 1401; https://doi.org/10.3390/antiox10091401 - 31 Aug 2021
Cited by 7 | Viewed by 2541
Abstract
Teleost fish are often regarded with interest for the remarkable ability of several species to tolerate even dramatic stresses, either internal or external, as in the case of fluctuations in O2 availability and temperature regimes. These events are naturally experienced by many [...] Read more.
Teleost fish are often regarded with interest for the remarkable ability of several species to tolerate even dramatic stresses, either internal or external, as in the case of fluctuations in O2 availability and temperature regimes. These events are naturally experienced by many fish species under different time scales, but they are now exacerbated by growing environmental changes. This further challenges the intrinsic ability of animals to cope with stress. The heart is crucial for the stress response, since a proper modulation of the cardiac function allows blood perfusion to the whole organism, particularly to respiratory organs and the brain. In cardiac cells, key signalling pathways are activated for maintaining molecular equilibrium, thus improving stress tolerance. In fish, the nitric oxide synthase (NOS)/nitric oxide (NO) system is fundamental for modulating the basal cardiac performance and is involved in the control of many adaptive responses to stress, including those related to variations in O2 and thermal regimes. In this review, we aim to illustrate, by integrating the classic and novel literature, the current knowledge on the NOS/NO system as a crucial component of the cardiac molecular mechanisms that sustain stress tolerance and adaptation, thus providing some species, such as tolerant cyprinids, with a high resistance to stress. Full article
(This article belongs to the Special Issue NOS/NO System and Heart)
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20 pages, 1596 KiB  
Review
Physical Exercise and Cardiac Repair: The Potential Role of Nitric Oxide in Boosting Stem Cell Regenerative Biology
by Fabiola Marino, Mariangela Scalise, Eleonora Cianflone, Luca Salerno, Donato Cappetta, Nadia Salerno, Antonella De Angelis, Daniele Torella and Konrad Urbanek
Antioxidants 2021, 10(7), 1002; https://doi.org/10.3390/antiox10071002 - 23 Jun 2021
Cited by 22 | Viewed by 3630
Abstract
Over the years strong evidence has been accumulated showing that aerobic physical exercise exerts beneficial effects on the prevention and reduction of cardiovascular risk. Exercise in healthy subjects fosters physiological remodeling of the adult heart. Concurrently, physical training can significantly slow-down or even [...] Read more.
Over the years strong evidence has been accumulated showing that aerobic physical exercise exerts beneficial effects on the prevention and reduction of cardiovascular risk. Exercise in healthy subjects fosters physiological remodeling of the adult heart. Concurrently, physical training can significantly slow-down or even reverse the maladaptive pathologic cardiac remodeling in cardiac diseases, improving heart function. The underlying cellular and molecular mechanisms of the beneficial effects of physical exercise on the heart are still a subject of intensive study. Aerobic activity increases cardiovascular nitric oxide (NO) released mainly through nitric oxidase synthase 3 activity, promoting endothelium-dependent vasodilation, reducing vascular resistance, and lowering blood pressure. On the reverse, an imbalance between increasing free radical production and decreased NO generation characterizes pathologic remodeling, which has been termed the “nitroso-redox imbalance”. Besides these classical evidence on the role of NO in cardiac physiology and pathology, accumulating data show that NO regulate different aspects of stem cell biology, including survival, proliferation, migration, differentiation, and secretion of pro-regenerative factors. Concurrently, it has been shown that physical exercise generates physiological remodeling while antagonizes pathologic remodeling also by fostering cardiac regeneration, including new cardiomyocyte formation. This review is therefore focused on the possible link between physical exercise, NO, and stem cell biology in the cardiac regenerative/reparative response to physiological or pathological load. Cellular and molecular mechanisms that generate an exercise-induced cardioprotective phenotype are discussed in regards with myocardial repair and regeneration. Aerobic training can benefit cells implicated in cardiovascular homeostasis and response to damage by NO-mediated pathways that protect stem cells in the hostile environment, enhance their activation and differentiation and, in turn, translate to more efficient myocardial tissue regeneration. Moreover, stem cell preconditioning by and/or local potentiation of NO signaling can be envisioned as promising approaches to improve the post-transplantation stem cell survival and the efficacy of cardiac stem cell therapy. Full article
(This article belongs to the Special Issue NOS/NO System and Heart)
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