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Antioxidants
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Oxidative Stress in Cardiorenal System
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Oxidative Stress in Cardiorenal System

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 (20 September 2023) | Viewed by 14490

Special Issue Editors

Dr. Carlos Renato Tirapelli

E-Mail Website1 Website2
Guest Editor
Laboratory of Pharmacology, College of Nursing of Ribeirão Preto, University of Sao Paulo, Sao Paulo, Brazil
Interests: oxidative stress; cardiovascular; endothelium; perivascular adipose tissue; reactive oxygen species
Dr. Júlio César Padovan

E-Mail Website
Guest Editor
Laboratory of Blood and Vascular Biology, The Rockefeller University, New York, NY 10065, USA
Interests: platelets; integrins; aggregation; clot formation; fibrin/fibrinogen; mass spectrometry; bioinformatics

Special Issue Information

Dear Colleagues,

Reactive oxygen species (ROS) play an important role in the pathogenesis of cardiovascular and renal diseases in that they contribute to the development of cardiorenal complications including endothelial dysfunction, inflammation, remodeling, apoptosis, cell migration, and activation of adhesion molecules. These events are significant to the pathogeneses of hypertension, obesity, atherosclerosis, diabetes mellitus and other conditions that affect the cardiorenal system. Many enzymatic systems in the kidney, heart and blood vessels may contribute to ROS generation, including nicotinamide adenine dinucleotide phosphate (NADPH) oxidase, mitochondrial enzymes and uncoupled endothelial nitric oxide (NO) synthase (eNOS). Among the ROS generated in such organs, superoxide (O2•-) and hydrogen peroxide (H2O2) are especially important for their association to elevations in intracellular calcium levels, reduction in nitric oxide (NO) bioavailability, lipoperoxidation, and the activation of redox-signaling pathways, which all lead to cardiorenal dysfunction in many pathologies.

We invite you to submit your latest research findings or a review article to this Special Issue, which will bring together current research concerning the role of oxidative stress in the genesis and maintenance of cardiorenal dysfunction in distinctive diseased states. The research can include both in vitro and in vivo studies relating to the role of oxidative stress in the pathogenesis of disease processes related to the cardiovascular and renal systems. We believe this Special Issue will provide scientifically innovative publications, stimulating wider discussion in the field.

We look forward to your contribution.

Dr. Carlos Renato Tirapelli
Dr. Júlio César Padovan
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

  • reactive oxygen species (ROS)
  • cardiovascular
  • cardiorenal
  • oxidative stress
  • NADPH oxidase
  • pathogenesis

Published Papers (7 papers)

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Research

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21 pages, 4135 KiB  
Article
Vasodilator Responses of Perivascular Adipose Tissue-Derived Hydrogen Sulfide Stimulated with L-Cysteine in Pregnancy Hypertension-Induced Endothelial Dysfunction in Rats
by Priscilla Bianca de Oliveira, Gabriela Palma Zochio, Edileia Souza Paula Caetano, Maria Luiza Santos da Silva and Carlos Alan Dias-Junior
Antioxidants 2023, 12(11), 1919; https://doi.org/10.3390/antiox12111919 - 26 Oct 2023
Viewed by 1149
Abstract
Endothelium-derived nitric oxide (NO)-induced vasodilation is impaired in pregnancy hypertension. However, the role of perivascular adipose tissue (PVAT)-derived hydrogen sulfide (H2S), as an alternative for counteracting vascular dysfunction, is incompletely clear in hypertensive disorders of pregnancy. Therefore, PVAT-derived H2S-induced [...] Read more.
Endothelium-derived nitric oxide (NO)-induced vasodilation is impaired in pregnancy hypertension. However, the role of perivascular adipose tissue (PVAT)-derived hydrogen sulfide (H2S), as an alternative for counteracting vascular dysfunction, is incompletely clear in hypertensive disorders of pregnancy. Therefore, PVAT-derived H2S-induced vasodilation was investigated in pregnancy hypertension-induced endothelial dysfunction. Non-pregnant (Non-Preg) and pregnant (Preg) rats were submitted (or not) to the deoxycorticosterone (DOCA)-salt protocol and assigned as follows (n = 10/group): Non-Preg, Non-Preg+DOCA, Preg, and Preg+DOCA groups. Systolic blood pressure (SBP), angiogenesis-related factors, determinant levels of H2S (PbS), NO (NOx), and oxidative stress (MDA) were assessed. Vascular changes were recorded in thoracic aortas with PVAT and endothelium (intact and removed layers). Vasorelaxation responses to the substrate (L-cysteine) for the H2S-producing enzyme cystathionine-γ-lyase (CSE) were examined in the absence and presence of CSE-inhibitor DL-propargylglycine (PAG) in thoracic aorta rings pre-incubated with cofactor for CSE (pyridoxal-5 phosphate: PLP) and pre-contracted with phenylephrine. Hypertension was only found in the Preg+DOCA group. Preg+DOCA rats showed angiogenic imbalances and increased levels of MDA. PbS, but not NOx, showed increased levels in the Preg+DOCA group. Pre-incubation with PLP and L-cysteine elevated determinants of H2S in PVAT and placentas of Preg-DOCA rats, whereas no changes were found in the aortas without PVAT. Aortas of Preg-DOCA rats showed that PVAT-derived H2S-dependent vasodilation was greater compared to endothelium-derived H2S, whereas PAG blocked these responses. PVAT-derived H2S endogenously stimulated with the amino acid L-cysteine may be an alternative to induce vasorelaxation in endothelial dysfunction related to pregnancy hypertension. Full article
(This article belongs to the Special Issue Oxidative Stress in Cardiorenal System)
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21 pages, 5198 KiB  
Article
A Rodent Model of Human-Dose-Equivalent 5-Fluorouracil: Toxicity in the Liver, Kidneys, and Lungs
by Mariana Conceição da Silva, Lilian Catarim Fabiano, Karile Cristina da Costa Salomão, Pedro Luiz Zonta de Freitas, Camila Quaglio Neves, Stephanie Carvalho Borges, Maria das Graças de Souza Carvalho, Ana Cristina Breithaupt-Faloppa, André Alexandre de Thomaz, Aline Mara dos Santos and Nilza Cristina Buttow
Antioxidants 2023, 12(5), 1005; https://doi.org/10.3390/antiox12051005 - 26 Apr 2023
Cited by 5 | Viewed by 2279
Abstract
5-Fluorouracil (5-FU) is a chemotherapy drug widely used to treat a range of cancer types, despite the recurrence of adverse reactions. Therefore, information on its side effects when administered at a clinically recommended dose is relevant. On this basis, we examined the effects [...] Read more.
5-Fluorouracil (5-FU) is a chemotherapy drug widely used to treat a range of cancer types, despite the recurrence of adverse reactions. Therefore, information on its side effects when administered at a clinically recommended dose is relevant. On this basis, we examined the effects of the 5-FU clinical treatment on the integrity of the liver, kidneys, and lungs of rats. For this purpose, 14 male Wistar rats were divided into treated and control groups and 5-FU was administered at 15 mg/kg (4 consecutive days), 6 mg/kg (4 alternate days), and 15 mg/kg on the 14th day. On the 15th day, blood, liver, kidney, and lung samples were collected for histological, oxidative stress, and inflammatory evaluations. We observed a reduction in the antioxidant markers and an increase in lipid hydroperoxides (LOOH) in the liver of treated animals. We also detected elevated levels of inflammatory markers, histological lesions, apoptotic cells, and aspartate aminotransferase. Clinical treatment with 5-FU did not promote inflammatory or oxidative alterations in the kidney samples; however, histological and biochemical changes were observed, including increased serum urea and uric acid. 5-FU reduces endogenous antioxidant defenses and increases LOOH levels in the lungs, suggesting oxidative stress. Inflammation and histopathological alterations were also detected. The clinical protocol of 5-FU promotes toxicity in the liver, kidneys, and lungs of healthy rats, resulting in different levels of histological and biochemical alterations. These results will be useful in the search for new adjuvants to attenuate the adverse effects of 5-FU in such organs. Full article
(This article belongs to the Special Issue Oxidative Stress in Cardiorenal System)
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14 pages, 2429 KiB  
Article
Pravastatin Prevents Increases in Activity of Metalloproteinase-2 and Oxidative Stress, and Enhances Endothelium-Derived Nitric Oxide-Dependent Vasodilation in Gestational Hypertension
by Cristal Jesus Toghi, Laisla Zanetoni Martins, Leonardo Lopes Pacheco, Edileia Souza Paula Caetano, Bruna Rahal Mattos, Elen Rizzi and Carlos Alan Dias-Junior
Antioxidants 2023, 12(4), 939; https://doi.org/10.3390/antiox12040939 - 16 Apr 2023
Cited by 2 | Viewed by 1682
Abstract
Pre-eclampsia (PE) is a hypertensive disorder of pregnancy and has been associated with placental growth restriction. The pre-eclamptic placenta releases free radicals to maternal circulation, thus increasing oxidative stress. An impaired redox state leads to reduction in circulating nitric oxide (NO) levels and [...] Read more.
Pre-eclampsia (PE) is a hypertensive disorder of pregnancy and has been associated with placental growth restriction. The pre-eclamptic placenta releases free radicals to maternal circulation, thus increasing oxidative stress. An impaired redox state leads to reduction in circulating nitric oxide (NO) levels and activation of extracellular matrix metalloproteinases (MMPs). However, activation of MMPs induced by oxidative stress is still unclear in PE. Antioxidant effects have been demonstrated with the use of pravastatin. Therefore, we hypothesized that pravastatin protects against oxidative stress-induced activation of MMPs in a rat model of PE. The animals were divided into four groups: normotensive pregnant rats (Norm-Preg); pregnant rats treated with pravastatin (Norm-Preg + Prava); hypertensive pregnant rats (HTN-Preg); and hypertensive pregnant rats treated with pravastatin (HTN-Preg + Prava). The deoxycorticosterone acetate (DOCA) and sodium chloride (DOCA-salt) model was used to induce hypertension in pregnancy. Blood pressure, and fetal and placental parameters were recorded. The gelatinolytic activity of MMPs, NO metabolites and lipid peroxide levels were also determined. Endothelium function was also examined. Pravastatin attenuated maternal hypertension, prevented placental weight loss, increased NO metabolites, inhibited increases in lipid peroxide levels, and reduced the activity of MMP-2, and these effects were observed along with enhanced endothelium-derived NO-dependent vasodilation. The present results provide evidence that pravastatin protects against activation of MMP-2 induced by oxidative stress in pre-eclamptic rats. These findings may also involve improvement in endothelial function related to NO and antihypertensive effects of pravastatin, thus suggesting pravastatin as a therapeutic intervention for PE. Full article
(This article belongs to the Special Issue Oxidative Stress in Cardiorenal System)
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Review

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17 pages, 1952 KiB  
Review
XBP1 Modulates the Aging Cardiorenal System by Regulating Oxidative Stress
by Ji Zhang, Yuanyuan Zhao and Nianqiao Gong
Antioxidants 2023, 12(11), 1933; https://doi.org/10.3390/antiox12111933 - 30 Oct 2023
Cited by 1 | Viewed by 1162
Abstract
X-box binding protein 1 (XBP1) is a unique basic-region leucine zipper (bZIP) transcription factor. Over recent years, the powerful biological functions of XBP1 in oxidative stress have been gradually revealed. When the redox balance remains undisturbed, oxidative stress plays a role in physiological [...] Read more.
X-box binding protein 1 (XBP1) is a unique basic-region leucine zipper (bZIP) transcription factor. Over recent years, the powerful biological functions of XBP1 in oxidative stress have been gradually revealed. When the redox balance remains undisturbed, oxidative stress plays a role in physiological adaptations and signal transduction. However, during the aging process, increased cellular senescence and reduced levels of endogenous antioxidants cause an oxidative imbalance in the cardiorenal system. Recent studies from our laboratory and others have indicated that these age-related cardiorenal diseases caused by oxidative stress are guided and controlled by a versatile network composed of diversified XBP1 pathways. In this review, we describe the mechanisms that link XBP1 and oxidative stress in a range of cardiorenal disorders, including mitochondrial instability, inflammation, and alterations in neurohumoral drive. Furthermore, we propose that differing degrees of XBP1 activation may cause beneficial or harmful effects in the cardiorenal system. Gaining a comprehensive understanding of how XBP1 exerts influence on the aging cardiorenal system by regulating oxidative stress will enhance our ability to provide new directions and strategies for cardiovascular and renal safety outcomes. Full article
(This article belongs to the Special Issue Oxidative Stress in Cardiorenal System)
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25 pages, 1312 KiB  
Review
Reactive Oxygen Species Are Central Mediators of Vascular Dysfunction and Hypertension Induced by Ethanol Consumption
by Júlio C. Padovan, Thales M. H. Dourado, Gustavo F. Pimenta, Thiago Bruder-Nascimento and Carlos R. Tirapelli
Antioxidants 2023, 12(10), 1813; https://doi.org/10.3390/antiox12101813 - 29 Sep 2023
Cited by 1 | Viewed by 1442
Abstract
Consumption of high amounts of ethanol is a risk factor for development of cardiovascular diseases such as arterial hypertension. The hypertensive state induced by ethanol is a complex multi-factorial event, and oxidative stress is a pathophysiological hallmark of vascular dysfunction associated with ethanol [...] Read more.
Consumption of high amounts of ethanol is a risk factor for development of cardiovascular diseases such as arterial hypertension. The hypertensive state induced by ethanol is a complex multi-factorial event, and oxidative stress is a pathophysiological hallmark of vascular dysfunction associated with ethanol consumption. Increasing levels of reactive oxygen species (ROS) in the vasculature trigger important processes underlying vascular injury, including accumulation of intracellular Ca2+ ions, reduced bioavailability of nitric oxide (NO), activation of mitogen-activated protein kinases (MAPKs), endothelial dysfunction, and loss of the anticontractile effect of perivascular adipose tissue (PVAT). The enzyme nicotinamide adenine dinucleotide phosphate (NADPH) oxidase plays a central role in vascular ROS generation in response to ethanol. Activation of the renin–angiotensin–aldosterone system (RAAS) is an upstream mechanism which contributes to NADPH oxidase stimulation, overproduction of ROS, and vascular dysfunction. This review discusses the mechanisms of vascular dysfunction induced by ethanol, detailing the contribution of ROS to these processes. Data examining the association between neuroendocrine changes and vascular oxidative stress induced by ethanol are also reviewed and discussed. These issues are of paramount interest to public health as ethanol contributes to blood pressure elevation in the general population, and it is linked to cardiovascular conditions and diseases. Full article
(This article belongs to the Special Issue Oxidative Stress in Cardiorenal System)
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29 pages, 4793 KiB  
Review
Oxidative Stress, Reductive Stress and Antioxidants in Vascular Pathogenesis and Aging
by Mitko Mladenov, Lubomir Lubomirov, Olaf Grisk, Dimiter Avtanski, Vadim Mitrokhin, Iliyana Sazdova, Milena Keremidarska-Markova, Yana Danailova, Georgi Nikolaev, Rossitza Konakchieva and Hristo Gagov
Antioxidants 2023, 12(5), 1126; https://doi.org/10.3390/antiox12051126 - 19 May 2023
Cited by 9 | Viewed by 4677
Abstract
This review is focused on the mechanisms that regulate health, disease and aging redox status, the signal pathways that counteract oxidative and reductive stress, the role of food components and additives with antioxidant properties (curcumin, polyphenols, vitamins, carotenoids, flavonoids, etc.), and the role [...] Read more.
This review is focused on the mechanisms that regulate health, disease and aging redox status, the signal pathways that counteract oxidative and reductive stress, the role of food components and additives with antioxidant properties (curcumin, polyphenols, vitamins, carotenoids, flavonoids, etc.), and the role of the hormones irisin and melatonin in the redox homeostasis of animal and human cells. The correlations between the deviation from optimal redox conditions and inflammation, allergic, aging and autoimmune responses are discussed. Special attention is given to the vascular system, kidney, liver and brain oxidative stress processes. The role of hydrogen peroxide as an intracellular and paracrine signal molecule is also reviewed. The cyanotoxins β-N-methylamino-l-alanine (BMAA), cylindrospermopsin, microcystins and nodularins are introduced as potentially dangerous food and environment pro-oxidants. Full article
(This article belongs to the Special Issue Oxidative Stress in Cardiorenal System)
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Other

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11 pages, 993 KiB  
Hypothesis
The Combined Treatment of Glutathione Sodium Salt and Ascorbic Acid for Preventing Contrast-Associated Acute Kidney Injury in ST-Elevation Myocardial Infarction Patients Undergoing Primary PCI: A Hypothesis to Be Validated
by Alessio Arrivi, Giovanni Truscelli, Giacomo Pucci, Francesco Barillà, Roberto Carnevale, Cristina Nocella, Martina Sordi, Marcello Dominici, Gaetano Tanzilli and Enrico Mangieri
Antioxidants 2023, 12(3), 773; https://doi.org/10.3390/antiox12030773 - 22 Mar 2023
Cited by 3 | Viewed by 1457
Abstract
The occurrence of Contrast-Associated Acute Kidney Injury (CA-AKI) in patients with ST-Elevation Myocardial Infarction (STEMI) has a negative impact on the length of hospital stay and mortality. Reactive Oxygen Species (ROS) release, along with vasoconstriction and hypoperfusion, play a key role in its [...] Read more.
The occurrence of Contrast-Associated Acute Kidney Injury (CA-AKI) in patients with ST-Elevation Myocardial Infarction (STEMI) has a negative impact on the length of hospital stay and mortality. Reactive Oxygen Species (ROS) release, along with vasoconstriction and hypoperfusion, play a key role in its development. To date, there is still no validated prophylactic therapy for this disease. The use of antioxidants, based on experimental and clinical studies, looks promising. Taking into consideration previous literature, we speculate that an early, combined and prolonged intravenous administration of both Glutathione (GSH) and ascorbic acid in STEMI patients undergoing primary Percutaneous Coronary Intervention (pPCI) may be of value in counteracting the occurrence of CA-AKI. We aimed at evaluating this hypothesis by applying a multicenter research protocol, using a double-blind randomized, placebo-controlled trial design. The primary endpoint will be to test the efficacy of this combined antioxidant therapy in reducing the occurrence of renal damage, in patients with acute myocardial infarction treated with pPCI. Furthermore, we will investigate the effect of the study compounds on changes in oxidative stress markers and platelet activation levels through bio-humoral analyses. Full article
(This article belongs to the Special Issue Oxidative Stress in Cardiorenal System)
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