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Special Issue "Antioxidant Therapy for Cardiovascular Diseases"

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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: 31 March 2024 | Viewed by 8238

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Special Issue Editors

Dr. Lanrong Bi

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Guest Editor

Department of Chemistry, Michigan Technological University, Houghton, MI 49931, USA
Interests: development of novel molecular probes for DNA sequencing analysis and disease gene discovery; development of new imaging and therapeutic agents towards cancer and cardiovascular disease; design and synthesis of novel prodrugs of peptides and peptide mimetics
Special Issues, Collections and Topics in MDPI journals

Prof. Dr. K. Michael Gibson
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Guest Editor

Department of Pharmacotherapy, Washington State University, Pullman, WA 99164, USA
Interests: Professor Gibson’s research focus includes understanding the pathophysiology of selected disorders and developing novel pre-clinical treatment approaches with translational relevance.

Prof. Dr. Guim Kwon

E-Mail Website
Guest Editor

Department of Pharmaceutical Sciences, Southern Illinois University Edwardsville, Edwardsville, IL 62026, USA
Interests: diabetes; insulin; pancreatic beta cell; artificial pancreas system; glucose-insulin homeostasis

Special Issue Information

Dear Colleagues,

Cardiovascular oxidative damage occurs when endogenous antioxidant levels are too insufficient to neutralize reactive oxygen species (ROS) and associated free radicals. ROS is associated with the pathophysiology of cardiovascular disorders, including cardiac hypertrophy, cardiomyopathy, heart failure, ventricular remodeling, and myocardial infarction. Due to its high energetic demand, the heart has the highest rate of production of ROS, yet in comparison to other mammalian organs, the heart has a significantly lower level of antioxidants and total antioxidant enzyme activities. It is widely agreed that ROS and oxidative damage are pathological components of cardiovascular diseases (CVDs). Historically, free radicals were merely considered toxins that induce oxidative stress and concomitant cellular damage, and for decades, considerable research has focused on approaches to eliminate excess free radicals generated in the body. Yet, experimental and clinical studies focused on the use of antioxidant therapy to mitigate myocardial damage have yielded mixed results. Moreover, decreasing the systemic level of ROS by using antioxidant therapy may in fact be detrimental in certain instances. Homeostatic mechanisms that maintain the balance between ROS generation and antioxidant production and consumption in CVD require fine tuning for optimal therapeutic outcomes. Our objectives in this Special Issue of Antioxidants are twofold: 1) to re-evaluate the utility and value of antioxidants in the prevention and treatment of CVD; 2) to highlight the expanding efficacy of naturally occurring antioxidants and synthetic antioxidants toward improvement of the functional and structural changes of CVD.

As Guest Editors, we invite you to contribute to the Special Issue on “Antioxidant Therapy for Cardiovascular Diseases”. Original research reports and reviews will be published online in Antioxidants.

Dr. Lanrong Bi
Prof. Dr. K. Michael Gibson
Prof. Dr. Guim Kwon
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

Oxidative stress
Free radicals
Antioxidant
Cardiovascular diseases

Published Papers (5 papers)

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Research

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Open AccessArticle

A Sex-Specific Comparative Analysis of Oxidative Stress Biomarkers Predicting the Risk of Cardiovascular Events and All-Cause Mortality in the General Population: A Prospective Cohort Study

Martin F. Bourgonje

Amaal E. Abdulle

Lyanne M. Kieneker

Sacha la Bastide-van Gemert

and

Antioxidants 2023, 12(3), 690; https://doi.org/10.3390/antiox12030690 - 10 Mar 2023

Viewed by 1269

Abstract

Oxidative stress plays a pivotal role in cardiovascular (CV) disease, but current biomarkers used to predict CV events are still insufficient. In this study, we comparatively assessed the utility of redox-related biomarkers in predicting the risk of CV events and all-cause mortality in male and female subjects from the general population. Subjects (n = 5955) of the Prevention of REnal and Vascular ENd-stage Disease (PREVEND) population-based cohort study were included. Blood homocysteine, gamma-GT, HDL cholesterol, bilirubin and protein-adjusted free thiol (R-SH, sulfhydryl groups) levels were quantified at baseline and were prospectively analyzed in association with the risk of CV events and all-cause mortality. After adjustment for potentially confounding factors, protein-adjusted R-SH and homocysteine levels were significantly associated with the risk of CV events in men (HR 0.63 [0.40–0.99], p = 0.045 and HR 1.58 [1.20–2.08], p = 0.001, respectively). Protein-adjusted R-SH and HDL cholesterol levels were significantly associated with the risk of all-cause mortality in men (HR 0.52 [0.32–0.85], p = 0.009 and HR 0.90 [0.85–0.94], p < 0.001, respectively), while the same was observed for bilirubin and homocysteine levels in women (HR 0.68 [0.48–0.98], p = 0.040 and HR 2.30 [1.14–3.76], p < 0.001, respectively). Lower levels of protein-adjusted R-SH were robustly associated with an increased risk of CV events and all-cause mortality in men. Our results highlight the value of R-SH levels in cardiovascular risk assessment and their potential significance as being amenable to therapeutic intervention, while reaffirming the importance of other oxidative stress-related biomarkers, such as homocysteine, HDL cholesterol and bilirubin. Full article

(This article belongs to the Special Issue Antioxidant Therapy for Cardiovascular Diseases)

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Open AccessArticle

Dihydromyricetin Attenuates Diabetic Cardiomyopathy by Inhibiting Oxidative Stress, Inflammation and Necroptosis via Sirtuin 3 Activation

and

Antioxidants 2023, 12(1), 200; https://doi.org/10.3390/antiox12010200 - 15 Jan 2023

Cited by 1 | Viewed by 1122

Abstract

Dihydromyricetin (DHY), the main flavonoid component in Ampelopsis grossedentata, has important benefits for health. The present study aimed to investigate the exact effects and possible mechanisms of DHY on diabetic cardiomyopathy (DCM). Male C57BL/6 mice and sirtuin 3 (SIRT3) knockout (SIRT3-KO) mice were injected with streptozotocin (STZ) to induce a diabetic model. Two weeks later, DHY (250 mg/kg) or carboxymethylcellulose (CMC) were administrated once daily by gavage for twelve weeks. We found that DHY alleviated fasting blood glucose (FBG) and triglyceride (TG) as well as glycosylated hemoglobin (HbA1c) levels; increased fasting insulin (FINS); improved cardiac dysfunction; ameliorated myocardial hypertrophy, fibrosis and injury; suppressed oxidative stress, inflammasome and necroptosis; but improved SIRT3 expression in STZ-induced mice. Neonatal rat cardiomyocytes were pre-treated with DHY (80 μM) with or without high glucose (HG) stimulation. The results showed that DHY attenuated cell damage but improved SIRT3 expression and inhibited oxidative stress, inflammasome and necroptosis in cardiomyocytes with high glucose stimulation. Moreover, the above protective effects of DHY on DCM were unavailable in SIRT3-KO mice, implying a promising medical potential of DHY for DCM treatment. In sum, DHY improved cardiac dysfunction; ameliorated myocardial hypertrophy, fibrosis and injury; and suppressed oxidative stress, inflammation and necroptosis via SIRT3 activation in STZ-induced diabetic mice, suggesting DHY may serve as a candidate for an agent to attenuate diabetic cardiomyopathy. Full article

(This article belongs to the Special Issue Antioxidant Therapy for Cardiovascular Diseases)

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Open AccessArticle

Lotus Bee Pollen Extract Inhibits Isoproterenol-Induced Hypertrophy via JAK2/STAT3 Signaling Pathway in Rat H9c2 Cells

and

Antioxidants 2023, 12(1), 88; https://doi.org/10.3390/antiox12010088 - 30 Dec 2022

Cited by 4 | Viewed by 1113

Abstract

Bee pollen possesses an anti-cardiomyocyte injury effect by reducing oxidative stress levels and inhibiting inflammatory response and apoptosis, but the possible effect mechanism has rarely been reported. This paper explores the effect of the extract of lotus bee pollen (LBPE) on cardiomyocyte hypertrophy (CH) and its mechanism. The main components of LBPE were identified via UPLC-QTOF MS. An isoproterenol-induced rat H9c2 CH model was subsequently used to evaluate the protection of LBPE on cells. LBPE (100, 250 and 500 μg∙mL⁻¹) reduced the surface area, total protein content and MDA content, and increased SOD activity and GSH content in CH model in a dose-dependent manner. Meanwhile, quantitative real-time PCR trials confirmed that LBPE reduced the gene expression levels of CH markers, pro-inflammatory cytokines and pro-apoptosis factors, and increased the Bcl-2 mRNA expression and Bcl-2/Bax ratio in a dose-dependent manner. Furthermore, target fishing, bioinformatics analysis and molecular docking suggested JAK2 could be a pivotal target protein for the main active ingredients in the LBPE against CH. Ultimately, Western blot (WB) trials confirmed that LBPE can dose-dependently inhibit the phosphorylation of JAK2 and STAT3. The results show that LBPE can protect against ISO-induced CH, possibly via targeting the JAK2/STAT3 pathway, also suggesting that LBPE may be a promising candidate against CH. Full article

(This article belongs to the Special Issue Antioxidant Therapy for Cardiovascular Diseases)

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Open AccessArticle

The Interplay of Sirtuin-1, LDL-Cholesterol, and HDL Function: A Randomized Controlled Trial Comparing the Effects of Energy Restriction and Atorvastatin on Women with Premature Coronary Artery Disease

Dalila Pinheiro Leal

Gustavo Henrique Ferreira Gonçalinho

Thauany Martins Tavoni

Karen Lika Kuwabara

Ana Paula Paccanaro

Fatima Rodrigues Freitas

Célia Maria Cassaro Strunz

Luiz Antonio Machado César

Raul Cavalcante Maranhão

and

Antonio de Padua Mansur

Antioxidants 2022, 11(12), 2363; https://doi.org/10.3390/antiox11122363 - 29 Nov 2022

Cited by 2 | Viewed by 1110

Abstract

Introduction: HDL function has gained prominence in the literature as there is a greater predictive capacity for risk in early coronary artery disease when compared to the traditional parameters. However, it is unclear how dietary energy restriction and atorvastatin influence HDL function. Methods: A randomized controlled trial with 39 women with early CAD divided into three groups (n = 13): energy restriction (30% of VET), atorvastatin (80 mg), and control. Analyses of traditional biochemical markers (lipid and glucose profile), circulating Sirt-1, and HDL function (lipid composition, lipid transfer, and antioxidant capacity). Results: Participants’ mean age was 50.5 ± 3.8 years. Energy restriction increased Sirt-1 by 63.6 pg/mL (95%CI: 1.5–125.7; p = 0.045) and reduced BMI by 0.8 kg/m² (95%CI: −1.349–−0.273; p = 0.004) in a manner independent of other cardiometabolic factors. Atorvastatin reduced LDL-c by 40.0 mg/dL (95%CI: −69.910–−10.1; p = 0.010). Increased Sirt-1 and reduced BMI were independently associated with reduced phospholipid composition of HDL (respectively, β = −0.071; CI95%:−0.136–−0.006; p = 0.033; β = 7.486; CI95%:0.350–14.622; p = 0.040). Reduction in BMI was associated with lower HDL-free cholesterol (β = 0.818; CI95%:0.044–1.593; p = 0.039). LDL-c reduction by statins was associated with reduced maximal lipid peroxide production rate of HDL (β = 0.002; CI95%:0.000–0.003; p = 0.022) and total conjugated diene generation (β = 0.001; CI95%:0.000–0.001; p = 0.029). Conclusion: This study showed that energy restriction and atorvastatin administration were associated with changes in lipid profile, serum Sirt-1 concentrations, and HDL function. Full article

(This article belongs to the Special Issue Antioxidant Therapy for Cardiovascular Diseases)

Review

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Open AccessReview

Oxidative Stress Related to Plasmalemmal and Mitochondrial Phosphate Transporters in Vascular Calcification

Nhung Thi Nguyen

Tuyet Thi Nguyen

and

Kyu-Sang Park

Antioxidants 2022, 11(3), 494; https://doi.org/10.3390/antiox11030494 - 02 Mar 2022

Cited by 6 | Viewed by 2489

Abstract

Inorganic phosphate (Pi) is essential for maintaining cellular function but excess of Pi leads to serious complications, including vascular calcification. Accumulating evidence suggests that oxidative stress contributes to the pathogenic progression of calcific changes. However, the molecular mechanism underlying Pi-induced reactive oxygen species (ROS) generation and its detrimental consequences remain unclear. Type III Na⁺-dependent Pi cotransporter, PiT-1/-2, play a significant role in Pi uptake of vascular smooth muscle cells. Pi influx via PiT-1/-2 increases the abundance of PiT-1/-2 and depolarization-activated Ca²⁺ entry due to its electrogenic properties, which may lead to Ca²⁺ and Pi overload and oxidative stress. At least four mitochondrial Pi transporters are suggested, among which the phosphate carrier (PiC) is known to be mainly involved in mitochondrial Pi uptake. Pi transport via PiC may induce hyperpolarization and superoxide generation, which may lead to mitochondrial dysfunction and endoplasmic reticulum stress, together with generation of cytosolic ROS. Increase in net influx of Ca²⁺ and Pi and their accumulation in the cytosol and mitochondrial matrix synergistically increases oxidative stress and osteogenic differentiation, which could be prevented by suppressing either Ca²⁺ or Pi overload. Therapeutic strategies targeting plasmalemmal and mitochondrial Pi transports can protect against Pi-induced oxidative stress and vascular calcification. Full article

(This article belongs to the Special Issue Antioxidant Therapy for Cardiovascular Diseases)

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