Research

10 pages, 1276 KiB

Open AccessArticle

Circulating Soluble ACE2 Plays an Independent Role to Protect against Vascular Damage in Diabetic Mice

by Chris Tikellis, Gardner N. Robinson, Carlos J. Rosado, Duygu Batu, Maria A. Zuniga-Gutierrez, Raelene J. Pickering and Merlin C. Thomas

Antioxidants 2022, 11(5), 987; https://doi.org/10.3390/antiox11050987 - 18 May 2022

Cited by 1 | Viewed by 1716

Abstract

Circulating levels of soluble ACE2 are increased by diabetes. Although this increase is associated with the presence and severity of cardiovascular disease, the specific role of soluble ACE2 in atherogenesis is unclear. Previous studies suggested that, like circulating ACE, soluble ACE2 plays a [...] Read more.

Circulating levels of soluble ACE2 are increased by diabetes. Although this increase is associated with the presence and severity of cardiovascular disease, the specific role of soluble ACE2 in atherogenesis is unclear. Previous studies suggested that, like circulating ACE, soluble ACE2 plays a limited role in vascular homeostasis. To challenge this hypothesis, we aimed to selectively increase circulating ACE2 and measure its effects on angiotensin II dependent atherogenesis. Firstly, in Ace2/ApoE DKO mice, restoration of circulating ACE2 with recombinant murine soluble (rmACE2_19-613; 1 mg/kg/alternate day IP) reduced plaque accumulation in the aortic arch, suggesting that the phenotype may be driven as much by loss of soluble ACE2 as the reduction in local ACE2. Secondly, in diabetic ApoE KO mice, where activation of the renin angiotensin system drives accelerated atherosclerosis, rmACE2_19-613 also reduced plaque accumulation in the aorta after 6 weeks. Thirdly, to ensure consistent long-term delivery of soluble ACE2, an intramuscular injection was used to deliver a DNA minicircle encoding ACE2_19-613. This strategy efficiently increased circulating soluble ACE2 and reduced atherogenesis and albuminuria in diabetic ApoE KO mice followed for 10 weeks. We propose that soluble ACE2 has independent vasculoprotective effects. Future strategies that increase soluble ACE2 may reduce accelerated atherosclerosis in diabetes and other states in which the renin angiotensin system is upregulated. Full article

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

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10 pages, 1619 KiB

Open AccessArticle

A Novel Combination of High-Load Omega-3 Lysine Complex (AvailOm^®) and Anthocyanins Exerts Beneficial Cardiovascular Effects

by Paola Di Pietro, Rosario Lizio, Carmine Izzo, Valeria Visco, Antonio Damato, Eleonora Venturini, Massimiliano De Lucia, Gennaro Galasso, Serena Migliarino, Barbara Rasile, Michele Ciccarelli, Carmine Vecchione and Albino Carrizzo

Antioxidants 2022, 11(5), 896; https://doi.org/10.3390/antiox11050896 - 30 Apr 2022

Cited by 6 | Viewed by 2144

Abstract

Omega-3 fatty acids have been shown to exert several beneficial effects in the prevention of cardiovascular and cerebrovascular diseases. The objective of the present study was to analyze the effects of a novel high-load omega-3 lysine complex, AvailOm^®, its related constituents [...] Read more.

Omega-3 fatty acids have been shown to exert several beneficial effects in the prevention of cardiovascular and cerebrovascular diseases. The objective of the present study was to analyze the effects of a novel high-load omega-3 lysine complex, AvailOm^®, its related constituents and a novel mixture of AvailOm^® with specific vasoactive anthocyanins on vascular function in mice resistance artery. Pressure myograph was used to perform vascular reactivity studies. Nitric oxide and oxidative stress were assessed by difluorofluorescein diacetate and dihydroethidium, respectively. Increasing doses of AvailOm^® exerted a dose-response vasorelaxation via AMPK-eNOS-mediated signaling. Omega-3 Ethyl Ester was identified as the main bioactive derivative of AvailOm^®, being capable of inducing vasorelaxant action to the same extent of entire product. The combination of AvailOm^® with a mix of potent vasoactive anthocyanins (C3-glu + DP3-glu + Mal3-glu + Mal3-gal + PEO3-gal), strongly protected mesenteric arteries from vascular dysfunction and oxidative stress evoked by oxidized-LDL. These data demonstrate for the first time the direct effects of AvailOm^® on resistance arteries. The evidence that the combination of specific vasoactive anthocyanins and AvailOm^® further enhanced the vasculoprotective properties of these compounds, may offer new promising perspectives for preventing the onset of cardiovascular and cerebrovascular events. Full article

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

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11 pages, 1003 KiB

Open AccessArticle

Mercaptoalbumin Is Associated with Graft Patency in Patients Undergoing Coronary Artery Bypass Grafting

by Maura Brioschi, Erica Gianazza, Daniele Andreini, Saima Mushtaq, Laura Cavallotti, Fabrizio Veglia, Calogero C. Tedesco, Gualtiero I. Colombo, Mauro Pepi, Gianluca Polvani, Elena Tremoli, Alessandro Parolari and Cristina Banfi

Antioxidants 2022, 11(4), 702; https://doi.org/10.3390/antiox11040702 - 02 Apr 2022

Viewed by 1743

Abstract

Coronary artery bypass graft (CABG) surgery still represents the gold standard for patients with complex multivessel coronary artery disease. However, graft occlusion still occurs in a significant proportion of CABG conduits, and oxidative stress is currently considered to be a potential contributor. Human [...] Read more.

Coronary artery bypass graft (CABG) surgery still represents the gold standard for patients with complex multivessel coronary artery disease. However, graft occlusion still occurs in a significant proportion of CABG conduits, and oxidative stress is currently considered to be a potential contributor. Human serum albumin (HSA) represents the main antioxidant in plasma through its reduced amino acid Cys34, which can efficiently scavenge several oxidants. In a nested case–control study including 36 patients with occluded grafts and 38 age- and sex-matched patients without occlusion, we assessed the levels of the native mercaptoalbumin (HSA-SH) and oxidized thiolated form of albumin (Thio-HSA) in relation with graft occlusion within 5 years after CABG. We found that the plasma level of preoperative HSA-SH was significantly lower in patients with occluded graft at 5 years follow-up than in patients with graft patency. Furthermore, low HSA-SH remained independently associated with graft occlusion even after adjusting for preoperative D-dimer, a well-known marker of activated coagulation recently found to be associated with graft occlusion. In conclusion, the preoperative level of HSA-SH is independently associated with graft occlusion in CABG and represents a measurable and potentially druggable predictor. Full article

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

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11 pages, 732 KiB

Open AccessArticle

by Francesco Versaci, Valentina Valenti, Maurizio Forte, Vittoria Cammisotto, Cristina Nocella, Simona Bartimoccia, Leonardo Schirone, Sonia Schiavon, Daniele Vecchio, Luca D’Ambrosio, Giulia Spinosa, Alessandra D’Amico, Isotta Chimenti, Francesco Violi, Giacomo Frati, Pasquale Pignatelli, Sebastiano Sciarretta, Daniele Pastori and Roberto Carnevale

Antioxidants 2022, 11(4), 698; https://doi.org/10.3390/antiox11040698 - 01 Apr 2022

Cited by 4 | Viewed by 2243

Abstract

Background: Aging is an independent risk factor for cardiovascular diseases. The autophagy process may play a role in delaying aging and improving cardiovascular function in aging. Data regarding autophagy in atrial fibrillation (AF) patients are lacking. Methods: A post hoc analysis of the [...] Read more.

Background: Aging is an independent risk factor for cardiovascular diseases. The autophagy process may play a role in delaying aging and improving cardiovascular function in aging. Data regarding autophagy in atrial fibrillation (AF) patients are lacking. Methods: A post hoc analysis of the prospective ATHERO-AF cohort study, including 150 AF patients and 150 sex- and age-matched control subjects (CS), was performed. For the analysis, the population was divided into three age groups: <50–60, 61–70, and >70 years. Oxidative stress (Nox2 activity and hydrogen peroxide, H₂O₂), platelet activation (PA) by sP-selectin and CD40L, endothelial dysfunction (nitric oxide, NO), and autophagy parameters (P62 and ATG5 levels) were assessed. Results: Nox2 activity and H₂O₂ production were higher in the AF patients than in the CS; conversely, antioxidant capacity was decreased in the AF patients compared to the CS, as was NO production. Moreover, sP-selectin and CD40L were higher in the AF patients than in the CS. The autophagy process was also significantly impaired in the AF patients. We found a significant difference in oxidative stress, PA, NO production, and autophagy across the age groups. Autophagy markers correlated with oxidative stress, PA, and endothelial dysfunction in both groups. Conclusions: This study provides evidence that the autophagy process may represent a mechanism for increased cardiovascular risk in the AF population. Full article

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

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26 pages, 7133 KiB

Open AccessArticle

Role of a Novel Silver Fir (Abies alba) Extract, Abigenol^®/AlbiPhenol^®, in Modulating Cardiovascular Disorders: Key Factors

by Kevin Leone, Marta Micheletto, Giovanni Di Maira, Erik Tedesco, Federico Benetti and Urška Zaloker

Antioxidants 2022, 11(4), 618; https://doi.org/10.3390/antiox11040618 - 23 Mar 2022

Cited by 3 | Viewed by 1796

Abstract

Cardiovascular diseases (CVDs) represent the leading cause of death worldwide, being responsible for about one third of deaths. Among CVDs, coronary artery diseases (CADs) are characterized by vascular endothelium dysfunction due to oxidative and inflammatory damages, the oxidation of circulating low-density lipoproteins (LDL) [...] Read more.

Cardiovascular diseases (CVDs) represent the leading cause of death worldwide, being responsible for about one third of deaths. Among CVDs, coronary artery diseases (CADs) are characterized by vascular endothelium dysfunction due to oxidative and inflammatory damages, the oxidation of circulating low-density lipoproteins (LDL) and high-density lipoproteins (HDL), and the production of ROS in the steatotic liver with the consequent increase of lipids and cholesterol. Together with CADs, heart failure (HF) represents another high-mortality rate CVD. A major risk factor for HF is hypertension that is accompanied by oxidative stress. Phytoextracts, rich in antioxidant and anti-inflammatory compounds, may have therapeutic value as they can interfere with several CVDs risk factors. In this work, a novel silver fir (Abies alba) bark extract, Abigenol^®/AlbiPhenol^®, was studied. First, Abigenol^®/AlbiPhenol^® cytotoxicity, bioaccessibility and bioavailability were evaluated by using an in vitro digestion model. Abigenol^®/AlbiPhenol^® was shown to be non-cytotoxic and showed good bioaccessibility. Then, by using in vitro hepatic, cardiac and vascular models, its antioxidant and anti-steatotic properties were assessed. Abigenol^®/AlbiPhenol^® showed an effective antioxidant action, and it was able to inhibit LDL and HDL oxidation, the main actors in atherosclerotic plaque formation. In steatotic conditions, Abigenol^®/AlbiPhenol^® induces decreased lipid and cholesterol accumulation in hepatocytes. In addition, in a cardiac model, the formulation reduced the activity of the hypertension-related angiotensin-converting enzyme (ACE). Altogether, these findings reveal a potential application of Abigenol^®/AlbiPhenol^® in the prevention and treatment of CVDs. Full article

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

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12 pages, 3048 KiB

Open AccessArticle

The Involvement of Sirtuin 1 Dysfunction in High-Fat Diet-Induced Vascular Dysfunction in Mice

by Ning Xia, Gisela Reifenberg, Christian Schirra and Huige Li

Antioxidants 2022, 11(3), 541; https://doi.org/10.3390/antiox11030541 - 12 Mar 2022

Cited by 7 | Viewed by 2079

Abstract

High-fat diet (HFD)-induced vascular impairment in mice is associated with a dysfunction of the perivascular adipose tissue (PVAT). The present study was conducted to investigate the involvement of sirtuin 1 (SIRT1). Male C57BL/6J mice were fed an HFD for 20 weeks to induce [...] Read more.

High-fat diet (HFD)-induced vascular impairment in mice is associated with a dysfunction of the perivascular adipose tissue (PVAT). The present study was conducted to investigate the involvement of sirtuin 1 (SIRT1). Male C57BL/6J mice were fed an HFD for 20 weeks to induce obesity. Vascular function was analyzed using a wire myograph system. In obese mice, the vasodilator response of PVAT-containing aortas to acetylcholine was reduced, although the vascular function of PVAT-free aortas remained normal. SIRT1 activity in PVAT of obese mice was reduced despite enhanced SIRT1 expression. Nicotinamide adenine dinucleotide (NAD⁺) levels and the NAD⁺/NADH ratio in the PVAT of obese mice were decreased, which was likely attributable to a downregulation of the NAD⁺-producing enzyme NAMPT. The reduced SIRT1 activity was associated with an enhanced acetylation of the endothelial nitric oxide synthase (eNOS) in the PVAT. Ex vivo incubation of PVAT-containing aorta from obese mice with NAD⁺ led to a complete normalization of vascular function. Thus, reduced SIRT1 activity due to NAD⁺ deficiency is involved in obesity-induced PVAT dysfunction. Full article

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

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13 pages, 3265 KiB

Open AccessArticle

Pequi Fruit Extract Increases Antioxidant Enzymes and Reduces Oxidants in Human Coronary Artery Endothelial Cells

by Karla M. S. Braga, Eugenio G. Araujo, Frank W. Sellke and M. Ruhul Abid

Antioxidants 2022, 11(3), 474; https://doi.org/10.3390/antiox11030474 - 28 Feb 2022

Cited by 3 | Viewed by 2241

Abstract

Reactive oxygen species (ROS) imbalance results in endothelial cell function impairment. Natural phenolic antioxidant compounds have been investigated as therapeutic alternatives. The fruit bark of Brazilian-native pequi (Caryocar brasiliense, Camb.) is rich in polyphenols. The HPLC-MS (High-Performance Liquid Chromatography coupled with [...] Read more.

Reactive oxygen species (ROS) imbalance results in endothelial cell function impairment. Natural phenolic antioxidant compounds have been investigated as therapeutic alternatives. The fruit bark of Brazilian-native pequi (Caryocar brasiliense, Camb.) is rich in polyphenols. The HPLC-MS (High-Performance Liquid Chromatography coupled with Mass Spectrometry) analyses identified gallic acid and catechin in six out of seven ethanolic extract samples prepared in our lab. In this study, we examined the effects of ethanolic pequi extract on ROS levels in human coronary artery endothelial cells (HCAEC) subjected to hypoxia or oxidative stress. We first confirmed the oxidant scavenging capacity of the extract. Then, HCAEC pre-incubated with 10 or 25 μg/mL of extract were subjected to hypoxia for 48 h or 100 μM H₂O₂ for six hours and compared to the normoxia group. Total and mitochondrial ROS levels and cell proliferation were measured. Pequi significantly reduced cytosolic HCAEC ROS levels in all conditions. Mitochondrial ROS were also reduced, except in hypoxia with 10 μg/mL of extract. HCAEC proliferation increased when treated with 25 μg/mL extract under hypoxia and after H₂O₂ addition. Additionally, pequi upregulated oxidative stress defense enzymes superoxide dismutase (SOD-)1, SOD-2, catalase, and glutathione peroxidase. Together, these findings demonstrate that pequi bark extract increases antioxidative enzyme levels, decreases ROS, and favors HACEC proliferation, pointing to a protective effect against oxidative stress. Full article

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

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14 pages, 1930 KiB

Open AccessEditor’s ChoiceArticle

N-Acetylcysteine Inhibits Platelet Function through the Regeneration of the Non-Oxidative Form of Albumin

by Sonia Eligini, Benedetta Porro, Giancarlo Aldini, Susanna Colli and Cristina Banfi

Antioxidants 2022, 11(3), 445; https://doi.org/10.3390/antiox11030445 - 23 Feb 2022

Cited by 8 | Viewed by 3223

Abstract

N-acetylcysteine (NAC) is able to break down protein disulfides, generating free thiols. This mechanism occurs on mixed disulfides of albumin (HSA) to form mercaptoalbumin (HMA), the main antioxidant species in the plasma. Circulating HSA exists in two main forms: the reduced form [...] Read more.

N-acetylcysteine (NAC) is able to break down protein disulfides, generating free thiols. This mechanism occurs on mixed disulfides of albumin (HSA) to form mercaptoalbumin (HMA), the main antioxidant species in the plasma. Circulating HSA exists in two main forms: the reduced form (HMA), and the oxidized forms, whose predominant modification is cystenylation (HSA-Cys). Increased levels of oxidized HSA have been detected in several diseases associated with oxidative stress. This study showed that NAC inhibits platelet aggregation by restoring HMA. In addition, the regeneration of HMA by NAC inhibits platelet functions such as intracellular calcium mobilization, reactive oxygen species generation, arachidonic acid metabolites synthesis, and adhesion to the collagen matrix. In our conditions, the exposure of platelets to NAC did not increase GSH levels. However, the inhibition of platelet aggregation was also detected following treatment of platelet-rich plasma with GSH, which, similarly to NAC, reduced HSA-Cys levels. Furthermore, this study showed that cysteine, another compound able to restore HMA by reducing the HSA-Cys content, inhibited platelet aggregation to a similar extent as NAC. The results obtained in this study suggest a new mechanism by which NAC can modulate platelet activation and suggest its possible use as an antiplatelet drug in conditions associated with oxidative stress. Full article

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

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23 pages, 868 KiB

Open AccessArticle

The Mutual Contribution of 3-NT, IL-18, Albumin, and Phosphate Foreshadows Death of Hemodialyzed Patients in a 2-Year Follow-Up

by Łukasz Kasprzak, Mateusz Twardawa, Piotr Formanowicz and Dorota Formanowicz

Antioxidants 2022, 11(2), 355; https://doi.org/10.3390/antiox11020355 - 11 Feb 2022

Cited by 2 | Viewed by 2277

Abstract

Patients with chronic kidney disease (CKD), especially those who are hemodialyzed (HD), are at significantly high risk of contracting cardiovascular disease and having increased mortality. This study aimed to find potential death predictors, the measurement of which may reflect increased mortality in HD [...] Read more.

Patients with chronic kidney disease (CKD), especially those who are hemodialyzed (HD), are at significantly high risk of contracting cardiovascular disease and having increased mortality. This study aimed to find potential death predictors, the measurement of which may reflect increased mortality in HD patients, and then combine the most promising ones in frames of a simple death risk assessment model. For this purpose, HD patients (

n = 71

) with acute myocardial infarction in the last year (HD group) and healthy people (control group) as a comparative group (

n = 32

) were included in the study. Various laboratory determinations and non-invasive cardiovascular tests were performed. Next, patients were followed for two years, and data on cardiovascular (CV) deaths were collected. On this basis, two HD groups were formed: patients who survived (HD-A,

n = 51

) and patients who died (HD-D,

n = 20

). To model HD mortality, 21 out of 90 potential variables collected or calculated from the raw data were selected. The best explanatory power (95.5%) was reached by a general linear model with four variables: interleukin 18, 3-nitrotyrosine, albumin, and phosphate. The interplay between immuno-inflammatory processes, nitrosative and oxidative stress, malnutrition, and calcium-phosphate disorders has been indicated to be essential in predicting CV-related mortality in studied HD patients. ClinicalTrials.gov Identifier: NCT05214872. Full article

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

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Review

Jump to: Research, Other

20 pages, 1311 KiB

Open AccessReview

Genetic Variations on Redox Control in Cardiometabolic Diseases: The Role of Nrf2

by Cecilia Zazueta, Alexis Paulina Jimenez-Uribe, José Pedraza-Chaverri and Mabel Buelna-Chontal

Antioxidants 2022, 11(3), 507; https://doi.org/10.3390/antiox11030507 - 06 Mar 2022

Cited by 9 | Viewed by 3031

Abstract

The transcription factor Nrf2 is a master regulator of multiple cytoprotective genes that maintain redox homeostasis and exert anti-inflammatory functions. The Nrf2-Keap1 signaling pathway is a paramount target of many cardioprotective strategies, because redox homeostasis is essential in cardiovascular health. Nrf2 gene variations, [...] Read more.

The transcription factor Nrf2 is a master regulator of multiple cytoprotective genes that maintain redox homeostasis and exert anti-inflammatory functions. The Nrf2-Keap1 signaling pathway is a paramount target of many cardioprotective strategies, because redox homeostasis is essential in cardiovascular health. Nrf2 gene variations, including single nucleotide polymorphisms (SNPs), are correlated with cardiometabolic diseases and drug responses. SNPs of Nrf2, KEAP1, and other related genes can impair the transcriptional activation or the activity of the resulting protein, exerting differential susceptibility to cardiometabolic disease progression and prevalence. Further understanding of the implications of Nrf2 polymorphisms on basic cellular processes involved in cardiometabolic diseases progression and prevalence will be helpful to establish more accurate protective strategies. This review provides insight into the association between the polymorphisms of Nrf2-related genes with cardiometabolic diseases. We also briefly describe that SNPs of Nrf2-related genes are potential modifiers of the pharmacokinetics that contribute to the inter-individual variability. Full article

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

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20 pages, 1057 KiB

Open AccessReview

Arterial Hypertension—Oxidative Stress and Inflammation

by Julia Krzemińska, Magdalena Wronka, Ewelina Młynarska, Beata Franczyk and Jacek Rysz

Antioxidants 2022, 11(1), 172; https://doi.org/10.3390/antiox11010172 - 17 Jan 2022

Cited by 45 | Viewed by 4132

Abstract

Arterial hypertension (AH) is a major cause of cardiovascular diseases (CVD), leading to dysfunction of many organs, including the heart, blood vessels and kidneys. AH is a multifactorial disease. It has been suggested that the development of each factor is influenced by oxidative [...] Read more.

Arterial hypertension (AH) is a major cause of cardiovascular diseases (CVD), leading to dysfunction of many organs, including the heart, blood vessels and kidneys. AH is a multifactorial disease. It has been suggested that the development of each factor is influenced by oxidative stress, which is characterized by a disturbed oxidant-antioxidant balance. Excessive production of reactive oxygen species (ROS) and an impaired antioxidant system promote the development of endothelial dysfunction (ED), inflammation and increased vascular contractility, resulting in remodeling of cardiovascular (CV) tissue. The hope for restoring the proper functioning of the vessels is placed on antioxidants, and pharmacological strategies are still being sought to reverse the harmful effects of free radicals. In our review, we focused on the correlation of AH with oxidative stress and inflammation, which are influenced by many factors, such as diet, supplementation and pharmacotherapy. Studies show that the addition of a single dietary component may have a beneficial effect on blood pressure (BP) values; however, the relationship between the antioxidant/anti-inflammatory properties of individual dietary components and the hypotensive effect is not clear. Moreover, AH pharmacotherapy alleviates the increased oxidative stress, which may help prevent organ damage. Full article

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

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14 pages, 827 KiB

Open AccessReview

Oxidative Stress in the Pathogenesis of Antiphospholipid Syndrome: Implications for the Atherothrombotic Process

by Cristina Nocella, Simona Bartimoccia, Vittoria Cammisotto, Alessandra D’Amico, Daniele Pastori, Giacomo Frati, Sebastiano Sciarretta, Paolo Rosa, Chiara Felici, Oliviero Riggio, Antonella Calogero, Roberto Carnevale and SMiLe Group

Antioxidants 2021, 10(11), 1790; https://doi.org/10.3390/antiox10111790 - 09 Nov 2021

Cited by 9 | Viewed by 4125

Abstract

Atherothrombosis is a frequent complication of the clinical history of patients with antiphospholipid syndrome (APS). Both atherothrombosis and APS are characterized by increased oxidative stress. Oxidative modifications are implicated in the formation of antiphospholipid antibodies, which in turn may favour the oxidative imbalance [...] Read more.

Atherothrombosis is a frequent complication of the clinical history of patients with antiphospholipid syndrome (APS). Both atherothrombosis and APS are characterized by increased oxidative stress. Oxidative modifications are implicated in the formation of antiphospholipid antibodies, which in turn may favour the oxidative imbalance by increasing the production of reactive oxidant species (ROS) or by a direct interaction with pro-oxidant/antioxidant enzymes. As a result of these processes, APS patients suffer from an oxidative imbalance that may contribute to the progression of the atherosclerotic process and to the onset of ischemic thrombotic complications. The aim of this review is to describe mechanisms implicated in the formation of ROS in APS patients and their involvement in the atherothrombotic process. We also provide an overview of potential therapeutic approaches to blunt oxidative stress and to prevent atherothrombotic complications in these patients. Full article

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

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Other

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42 pages, 1008 KiB

Open AccessSystematic Review

Systemic Inflammation, Oxidative Stress and Cardiovascular Health in Children and Adolescents: A Systematic Review

by Tjaša Hertiš Petek, Tadej Petek, Mirjam Močnik and Nataša Marčun Varda

Antioxidants 2022, 11(5), 894; https://doi.org/10.3390/antiox11050894 - 30 Apr 2022

Cited by 21 | Viewed by 3611

Abstract

Recent studies indicate that cerebrovascular diseases and processes of atherosclerosis originate in the childhood era and are largely influenced by chronic inflammation. Some features of vascular dysfunction in adulthood may even be programmed prenatally via genetic influences and an unfavorable intrauterine milieu. Oxidative [...] Read more.

Recent studies indicate that cerebrovascular diseases and processes of atherosclerosis originate in the childhood era and are largely influenced by chronic inflammation. Some features of vascular dysfunction in adulthood may even be programmed prenatally via genetic influences and an unfavorable intrauterine milieu. Oxidative stress, defined by an imbalance between the production and generation of reactive oxygen species (ROS) in cells and tissues and the capability of an organism to scavenge these molecules via antioxidant mechanisms, has been linked to adverse cardiovascular health in adults, yet has not been systematically reviewed in the pediatric population. We performed a systematic search as per the PRISMA guidelines in PubMed/Medline and Cochrane Reviews and detected, in total, 1228 potentially eligible pediatric articles on systemic inflammation, oxidative stress, antioxidant use, cardiovascular disease and endothelial dysfunction. The abstracts and full-text manuscripts of these were screened for inclusion and exclusion criteria, and a total of 160 articles were included. The results indicate that systemic inflammation and oxidative stress influence cardiovascular health in many chronic pediatric conditions, including hypertension, obesity, diabetes mellitus types 1 and 2, chronic kidney disease, hyperlipidemia and obstructive sleep apnea. Exercise and diet may diminish ROS formation and enhance the total serum antioxidant capacity. Antioxidant supplementation may, in selected conditions, contribute to the diminution of the oxidative state and improve endothelial function; yet, in many areas, studies provide unsatisfactory results. Full article

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

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