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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 August 2020) | Viewed by 55238

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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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Dear Colleagues,

Cardiovascular diseases are the leading cause of death worldwide, and the risk factors include smoking, high blood pressure, diet, high cholesterol, and diabetes. 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 byproduct 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. Further research is required not only to develop a better understanding of the mechanisms underlying oxidative stress and inflammation in cardiovascular disease but also to aid in the development of targeted interventions to combat both inflammation and oxidative stress.

We are inviting you to submit research or review articles to this Special Issue on oxidative stress and inflammation in cardiovascular diseases, which will be dedicated to providing further insight into recent developments in the field.

Prof. Raelene Pickering
Guest Editor

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Keywords

Cardiovascular Disease
Oxidative Stress
Inflammation
Reactive Oxygen Species

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Editorial

Jump to: Research, Review

2 pages, 163 KiB

Open AccessEditorial

Oxidative Stress and Inflammation in Cardiovascular Diseases

by Raelene J. Pickering

Antioxidants 2021, 10(2), 171; https://doi.org/10.3390/antiox10020171 - 25 Jan 2021

Cited by 16 | Viewed by 2928

Abstract

Cardiovascular diseases (CVD), which include a number of cardiac and vascular conditions, resulted in approximately 17 [...] Full article

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

Research

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15 pages, 4569 KiB

Open AccessArticle

Chronic Metabolic Acidosis Elicits Hypertension via Upregulation of Intrarenal Angiotensin II and Induction of Oxidative Stress

by Dinesh Aryal, Tithi Roy, Jean Christopher Chamcheu and Keith E. Jackson

Antioxidants 2021, 10(1), 2; https://doi.org/10.3390/antiox10010002 - 22 Dec 2020

Cited by 12 | Viewed by 3618

Abstract

Chronic metabolic acidosis (CMA) can be a consequence of persistent hypertension but could potentially play a role in invoking hypertension. Currently, there is a scarcity of studies examining the outcome of induced chronic acidosis on blood pressure regulation. This study investigates CMA as a cause of hypertension. Chronic acidosis was induced in Sprague Dawley rats (100–150 g) by providing a weak acid solution of 0.28 M ammonium chloride (NH₄Cl) in tap water for 8 weeks. To determine whether the rats were acidotic, blood pH was measured, while blood pressure (BP) was monitored by tail-cuff plethysmography weekly. Rats were divided into five groups: control, CMA, CMA ± spironolactone, captopril, and tempol. Serum sodium and potassium; renal interstitial fluid (for Angiotensin II concentration); and kidney proximal tubules (for Na⁺/K⁺ ATPase- α1 concentration) were analyzed. Reactive oxygen species (ROS) were detected in renal cortical homogenates using electron paramagnetic resonance (EPR). In the CMA rats, a sustained elevation in mean arterial pressure (MAP) associated with a significant decrease in blood pH was observed compared to that of control over the 8 weeks. A significant decrease in MAP was observed in acidotic rats treated with captopril/tempol, whereas spironolactone treatment caused no decrease in MAP as compared to that of the CMA group. The interstitial angiotensin II was increased in the CMA group but decreased in the CMA with captopril and tempol groups. In addition, the urinary sodium was decreased, and the serum sodium levels increased significantly in the CMA groups as compared to that of control. However, the acidotic groups with captopril and tempol showed reduced levels of serum sodium and an elevation in urinary sodium as compared to that of the CMA group. In addition, there was a significant increase in plasma renin and no change in plasma aldosterone in the CMA group with no significant differences in plasma renin or aldosterone observed during spironolactone, captopril, or tempol treatments. The increased expression of Na⁺/K⁺ ATPase-α1 in the CMA group suggests that active transport of Na⁺ to the blood could be causative of the observed hypertension. Furthermore, the EPR analysis confirmed an elevation in superoxide (O₂^-) radical levels in the CMA group, but the tempol/captopril treated acidotic groups showed less (O₂^-) compared to that of either the CMA group or control. Taken together, our data suggest that induction of CMA could potentially be causative of hypertension, while the mechanisms underlying the increased BP could be through the activation of intrarenal Ang II and induction of oxidative stress. Full article

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

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15 pages, 2436 KiB

Open AccessArticle

Oxidized Low-Density Lipoprotein Associates with Ventricular Stress in Young Adults and Triggers Intracellular Ca²⁺ Alterations in Adult Ventricular Cardiomyocytes

by Elena Rodríguez-Sánchez, José Alberto Navarro-García, Laura González-Lafuente, Jennifer Aceves-Ripoll, Sara Vázquez-Sánchez, Jonay Poveda, Elisa Mercado-García, Nerea Corbacho-Alonso, Eva Calvo-Bonacho, María Fernández-Velasco, Gloria Álvarez-Llamas, María G. Barderas, Luis M. Ruilope and Gema Ruiz-Hurtado

Antioxidants 2020, 9(12), 1213; https://doi.org/10.3390/antiox9121213 - 1 Dec 2020

Cited by 8 | Viewed by 3303

Abstract

Oxidized low-density lipoprotein (oxLDL) is associated with cardiac damage and causes injury to multiple cell types. We aimed to investigate the role of oxLDL in ventricular stress. We first examined the association between circulating oxLDL and N-terminal pro-brain natriuretic peptide (NT-proBNP), a marker of myocardial stress, in young subjects (30–50 years) with or without stable coronary artery disease (SCAD). oxLDL and NT-proBNP were significantly higher in subjects at high cardiovascular risk (CVR) than in subjects at low CVR and were associated independently of traditional CVR factors and C-reactive protein. Furthermore, the levels of oxLDL and NT-proBNP were significantly lower in subjects with SCAD than in peers at high CVR. To determine the intracellular mechanisms involved in the cardiac effects of oxLDL, we analyzed the in vitro effect of oxLDL on intracellular Ca²⁺ handling in adult rat ventricular cardiomyocytes using confocal microscopy. Acute challenge of adult ventricular cardiomyocytes to oxLDL reduced systolic Ca²⁺ transients and sarcoplasmic reticulum Ca²⁺ load. Moreover, diastolic spontaneous Ca²⁺ leak increased significantly after acute exposure to oxLDL. Thus, we demonstrate that oxLDL associates with NT-proBNP in young subjects, and can directly induce Ca²⁺ mishandling in adult ventricular cardiomyoyctes, predisposing cardiomyocytes to cardiac dysfunction and arrhythmogenicity. Full article

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

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20 pages, 5953 KiB

Open AccessArticle

Effects of Allicin on Pathophysiological Mechanisms during the Progression of Nephropathy Associated to Diabetes

by Abraham Said Arellano-Buendía, Luis Gerardo Castañeda-Lara, María L. Loredo-Mendoza, Fernando E. García-Arroyo, Pedro Rojas-Morales, Raúl Argüello-García, Juan G. Juárez-Rojas, Edilia Tapia, José Pedraza-Chaverri, Laura Gabriela Sánchez-Lozada and Horacio Osorio-Alonso

Antioxidants 2020, 9(11), 1134; https://doi.org/10.3390/antiox9111134 - 15 Nov 2020

Cited by 29 | Viewed by 5268

Abstract

This study aimed to assess the impact of allicin on the course of diabetic nephropathy. Study groups included control, diabetes, and diabetes-treated rats. Allicin treatment (16 mg/kg day/p.o.) started after 1 month of diabetes onset and was administered for 30 days. In the diabetes group, the systolic blood pressure (SBP) increased, also, the oxidative stress and hypoxia in the kidney cortex were evidenced by alterations in the total antioxidant capacity as well as the expression of nuclear factor (erythroid-derived 2)-like 2/Kelch ECH associating protein 1 (Nrf2/Keap1), hypoxia-inducible factor 1-alpha (HIF-1α), vascular endothelial growth factor (VEGF), erythropoietin (Epo) and its receptor (Epo-R). Moreover, diabetes increased nephrin, and kidney injury molecule-1 (KIM-1) expression that correlated with mesangial matrix, the fibrosis index and with the expression of connective tissue growth factor (CTGF), transforming growth factor-β1 (TGF-β1), and α-smooth muscle actin (α-SMA). The insulin levels and glucose transporter protein type-4 (GLUT4) expression were decreased; otherwise, insulin receptor substrates 1 and 2 (IRS-1 and IRS-2) expression was increased. Allicin increased Nrf2 expression and decreased SBP, Keap1, HIF-1α, and VEGF expression. Concurrently, nephrin, KIM-1, the mesangial matrix, fibrosis index, and the fibrotic proteins were decreased. Additionally, allicin decreased hyperglycemia, improved insulin levels, and prevented changes in (GLUT4) and IRSs expression induced by diabetes. In conclusion, our results demonstrate that allicin has the potential to help in the treatment of diabetic nephropathy. The cellular mechanisms underlying its effects mainly rely on the regulation of antioxidant, antifibrotic, and antidiabetic mechanisms, which can contribute towards delay in the progression of renal disease. Full article

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

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18 pages, 3159 KiB

Open AccessArticle

Activity of Antioxidants from Crocus sativus L. Petals: Potential Preventive Effects towards Cardiovascular System

by Keti Zeka, Pasquale Marrazzo, Matteo Micucci, Ketan C. Ruparelia, Randolph R. J. Arroo, Guido Macchiarelli, Stefania Annarita Nottola, Maria Adelaide Continenza, Alberto Chiarini, Cristina Angeloni, Silvana Hrelia and Roberta Budriesi

Antioxidants 2020, 9(11), 1102; https://doi.org/10.3390/antiox9111102 - 9 Nov 2020

Cited by 33 | Viewed by 4172

Abstract

The petals of the saffron crocus (Crocus sativus L.) are considered a waste material in saffron production, but may be a sustainable source of natural biologically active substances of nutraceutical interest. The aim of this work was to study the cardiovascular effects of kaempferol and crocin extracted from saffron petals. The antiarrhythmic, inotropic, and chronotropic effects of saffron petal extract (SPE), kaempferol, and crocin were evaluated through in vitro biological assays. The antioxidant activity of kaempferol and crocin was investigated through the 2′,7′-dichlorodihydrofluorescein diacetate (DCFH-DA) assay using rat cardiomyoblast cell line H9c2. The MTT assay was applied to assess the effects of kaempferol and crocin on cell viability. SPE showed weak negative inotropic and chronotropic intrinsic activities but a significant intrinsic activity on smooth muscle with a potency on the ileum greater than on the aorta: EC₅₀ = 0.66 mg/mL versus EC₅₀ = 1.45 mg/mL. Kaempferol and crocin showed a selective negative inotropic activity. In addition, kaempferol decreased the contraction induced by KCl (80 mM) in guinea pig aortic and ileal strips, while crocin had no effect. Furthermore, following oxidative stress, both crocin and kaempferol decreased intracellular ROS formation and increased cell viability in a concentration-dependent manner. The results indicate that SPE, a by-product of saffron cultivation, may represent a good source of phytochemicals with a potential application in the prevention of cardiovascular diseases. Full article

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

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26 pages, 3273 KiB

Open AccessArticle

Protective Effects of a Discontinuous Treatment with Alpha-Lipoic Acid in Obesity-Related Heart Failure with Preserved Ejection Fraction, in Rats

by Cristina Pop, Maria-Georgia Ștefan, Dana-Maria Muntean, Laurențiu Stoicescu, Adrian Florin Gal, Béla Kiss, Claudiu Morgovan, Felicia Loghin, Luc Rochette, Benjamin Lauzier, Cristina Mogoșan and Steliana Ghibu

Antioxidants 2020, 9(11), 1073; https://doi.org/10.3390/antiox9111073 - 31 Oct 2020

Cited by 20 | Viewed by 3638

Abstract

Obesity induces hemodynamic and humoral changes that are associated with functional and structural cardiac remodeling, which ultimately result in the development of heart failure (HF) with preserved ejection fraction (HFpEF). In recent years, pharmacological studies in patients with HFpEF were mostly unsatisfactory. In these conditions, alternative new therapeutic approaches are necessary. The aim of our study was (1) to assess the effects of obesity on heart function in an experimental model and (2) to evaluate the efficacy of an alpha-lipoic acid (ALA) antioxidant treatment. Sprague-Dawley rats (7 weeks old) were either included in the control group (n = 6) or subjected to abdominal aortic banding (AAB) and divided into three subgroups, depending on their diet: standard (AAB + SD, n = 8), hypecaloric (AAB + HD, n = 8) and hypecaloric with discontinuous ALA treatment (AAB + HD + ALA, n = 9). Body weight (BW), glycemia, echocardiography parameters and plasma hydroperoxides were monitored throughout the study. After 36 weeks, plasma adiposity (leptin and adiponectin) and inflammation (IL-6 and TNF-alpha) markers, together with B-type natriuretic peptide and oxidative stress markers (end-products of lipid peroxidation and endogenous antioxidant systems) were assessed. Moreover, cardiac fiber diameters were measured. In our experiment, diet-induced obesity generated cardiometabolic disturbances, and in association with pressure-overload induced by AAB, it precipitated the onset of heart failure, cardiac hypertrophy and diastolic dysfunction, while producing a pro-oxidant and pro-inflammatory plasmatic status. In relationship with its antioxidant effects, the chronic ALA-discontinuous treatment prevented BW gain and decreased metabolic and cardiac perturbations, confirming its protective effects on the cardiovascular system. Full article

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

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16 pages, 1246 KiB

Open AccessArticle

The Nitric Oxide System in Peripheral Artery Disease: Connection with Oxidative Stress and Biopterins

by Ahmed Ismaeel, Evlampia Papoutsi, Dimitrios Miserlis, Ramon Lavado, Gleb Haynatzki, George P. Casale, William T. Bohannon, Robert S. Smith, Jack Leigh Eidson, Robert Brumberg, Aaron Hayson, Jeffrey S. Kirk, Carlos Castro, Ian Sawicki, Charalambos Konstantinou, Luke P. Brewster, Iraklis I. Pipinos and Panagiotis Koutakis

Antioxidants 2020, 9(7), 590; https://doi.org/10.3390/antiox9070590 - 6 Jul 2020

Cited by 31 | Viewed by 4836

Abstract

Peripheral artery disease (PAD) pathophysiology extends beyond hemodynamics to include other operating mechanisms, including endothelial dysfunction. Oxidative stress may be linked to endothelial dysfunction by reducing nitric oxide (NO) bioavailability. We aimed to investigate whether the NO system and its regulators are altered in the setting of PAD and to assess the relationship between NO bioavailability and oxidative stress. Sera from 35 patients with intermittent claudication (IC), 26 patients with critical limb ischemia (CLI), and 35 non-PAD controls were analyzed to determine levels of tetrahydrobiopterin (BH4), dihydrobiopterin (BH2), nitrate/nitrite (nitric oxides, or NOx), arginine, citrulline, asymmetric dimethylarginine (ADMA), symmetric dimethylarginine (SDMA), and the oxidative stress markers 8-Oxo-2′-deoxyguanosine (8-OHdG), 4-hydroxynonenal (4-HNE), advanced glycation end products (AGEs), and protein carbonyls. NOx was significantly lower in IC and CLI patients compared to controls in association with elevated oxidative stress, with the greatest NOx reductions observed in CLI. Compared with controls, IC and CLI patients had reduced BH4, elevated BH2, and a reduced BH4/BH2 ratio. SDMA, the arginine/SDMA ratio, and the arginine/ADMA ratio were significantly higher in CLI patients. The NO system and its regulators are significantly compromised in PAD. This dysregulation appears to be driven by increased oxidative stress and worsens as the disease progresses from claudication to CLI. Full article

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

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14 pages, 1671 KiB

Open AccessArticle

Isosamidin from Peucedanum japonicum Roots Prevents Methylglyoxal-Induced Glucotoxicity in Human Umbilical Vein Endothelial Cells via Suppression of ROS-Mediated Bax/Bcl-2

by Moon Ho Do, Jae Hyuk Lee, Jongmin Ahn, Min Jee Hong, Jinwoong Kim and Sun Yeou Kim

Antioxidants 2020, 9(6), 531; https://doi.org/10.3390/antiox9060531 - 17 Jun 2020

Cited by 19 | Viewed by 3246

Abstract

Methylglyoxal (MGO) is a highly reactive metabolite of glucose. Elevated levels of MGO induce the generation of reactive oxygen species (ROS) and cause cell death in endothelial cells. Vascular endothelial cell damage by ROS has been implicated in the progression of diabetic vascular complications, cardiovascular diseases, and atherosclerosis. In this study, the protective effect of isosamidin, isolated from Peucedanum japonicum roots, on MGO-induced apoptosis was investigated using human umbilical vein endothelial cells (HUVECs). Among the 20 compounds isolated from P. japonicum, isosamidin showed the highest effectiveness in inhibiting MGO-induced apoptosis of HUVECs. Pretreatment of HUVECs with isosamidin significantly prevented the generation of ROS and cell death induced by MGO. Isosamidin prevented MGO-induced apoptosis in HUVECs by downregulating the expression of Bax and upregulating the expression of Bcl-2. MGO treatment activated mitogen-activated protein kinases (MAPKs), such as p38, c-Jun N terminal kinase (JNK), and extracellular signal-regulated kinase (ERK). In contrast, pretreatment with isosamidin strongly inhibited the activation of p38 and JNK. Furthermore, isosamidin caused the breakdown of the crosslinks of the MGO-derived advanced glycation end products (AGEs). These findings suggest that isosamidin from P. japonicum may be used as a preventive agent against MGO-mediated endothelial dysfunction in diabetes. However, further study of the therapeutic potential of isosamidin on endothelial dysfunction needs to explored in vivo models. Full article

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

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Review

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24 pages, 761 KiB

Open AccessReview

Oxidative Stress in ESRD Patients on Dialysis and the Risk of Cardiovascular Diseases

by Jacek Rysz, Beata Franczyk, Janusz Ławiński and Anna Gluba-Brzózka

Antioxidants 2020, 9(11), 1079; https://doi.org/10.3390/antiox9111079 - 3 Nov 2020

Cited by 38 | Viewed by 5714

Abstract

Chronic kidney disease is highly prevalent worldwide. The decline of renal function is associated with inadequate removal of a variety of uremic toxins that exert detrimental effects on cells functioning, thus affecting the cardiovascular system. The occurrence of cardiovascular aberrations in CKD is related to the impact of traditional risk factors and non-traditional CKD-associated risk factors, including anemia; inflammation; oxidative stress; the presence of some uremic toxins; and factors related to the type, frequency of dialysis and the composition of dialysis fluid. Cardiovascular diseases are the most frequent cause for the deaths of patients with all stages of renal failure. The kidney is one of the vital sources of antioxidant enzymes, therefore, the impairment of this organ is associated with decreased levels of these enzymes as well as increased levels of pro-oxidants. Uremic toxins have been shown to play a vital role in the onset of oxidative stress. Hemodialysis itself also enhances oxidative stress. Elevated oxidative stress has been demonstrated to be strictly related to kidney and cardiac damage as it aggravates kidney dysfunction and induces cardiac hypertrophy. Antioxidant therapies may prove to be beneficial since they can decrease oxidative stress, reduce uremic cardiovascular toxicity and improve survival. Full article

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

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54 pages, 1835 KiB

Open AccessReview

Chronic Kidney Disease as Oxidative Stress- and Inflammatory-Mediated Cardiovascular Disease

by Alina Podkowińska and Dorota Formanowicz

Antioxidants 2020, 9(8), 752; https://doi.org/10.3390/antiox9080752 - 14 Aug 2020

Cited by 186 | Viewed by 17508

Abstract

Generating reactive oxygen species (ROS) is necessary for both physiology and pathology. An imbalance between endogenous oxidants and antioxidants causes oxidative stress, contributing to vascular dysfunction. The ROS-induced activation of transcription factors and proinflammatory genes increases inflammation. This phenomenon is of crucial importance in patients with chronic kidney disease (CKD), because atherosclerosis is one of the critical factors of their cardiovascular disease (CVD) and increased mortality. The effect of ROS disrupts the excretory function of each section of the nephron. It prevents the maintenance of intra-systemic homeostasis and leads to the accumulation of metabolic products. Renal regulatory mechanisms, such as tubular glomerular feedback, myogenic reflex in the supplying arteriole, and the renin–angiotensin–aldosterone system, are also affected. It makes it impossible for the kidney to compensate for water–electrolyte and acid–base disturbances, which progress further in the mechanism of positive feedback, leading to a further intensification of oxidative stress. As a result, the progression of CKD is observed, with a spectrum of complications such as malnutrition, calcium phosphate abnormalities, atherosclerosis, and anemia. This review aimed to show the role of oxidative stress and inflammation in renal impairment, with a particular emphasis on its influence on the most common disturbances that accompany CKD. Full article

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

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