Free Radicals and Cardiovascular Diseases

A special issue of Antioxidants (ISSN 2076-3921).

Deadline for manuscript submissions: closed (30 November 2020) | Viewed by 22313

Special Issue Editors


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Guest Editor
Department of Physiology, Anatomy and Neuroscience, Interdisciplinary Excellence Centre, Faculty of Science and Informatics, University of Szeged, H-6726 Szeged, Hungary
Interests: myocardial adaptation; cardiovascular pharmacology; cardiovascular diseases; heme oxygenase
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Co-Guest Editor
Department of Physiology, Anatomy and Neuroscience, University of Szeged, H-6726 Szeged, Hungary
Interests: cardiovascular diseases; aging; lifestyle modifications; oxidative stress; inflammation
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Reactive oxygen species (ROS), including free radicals, play a pivotal role in the pathogenesis and development of cardiovascular diseases (CVDs); however, the underlying mechanisms have not been fully elucidated. A redox imbalance between production of free radicals and antioxidant capacity can cause oxidative damage affected by specific targets, such as inflammatory mediators, adhesion molecules, endothelial tissue, low-density lipoproteins (LDLs), leucocytes, and other factors. Their disturbance or alteration via intracellular signaling pathways can promote acute or chronic changes in the cardiovascular system. Due to the multifactorial influence of oxidative stress in CVD genesis and the numerous interlinked cellular cascades, novel integrative approaches may reveal new insights into the basis, progression, and treatment of CVD pathophysiology.

We invite investigators to contribute research papers, as well as review articles, that develop our understanding of ROS-dependent signaling mechanisms and new therapeutic targets against CVDs. Potential topics include, but are not limited to:

  • intracellular signaling cascades and redox-sensitive transcription factors, targeting free radicals and antioxidants, that contribute to our understanding of the mechanisms of CVDs;
  • identifying new biological pathways (e.g., the endocannabinoid system) that underlie cardiovascular complications mediated by ROS;
  • therapeutic interventions against CVDs, such as pharmacological and genetic antioxidant therapy; and
  • exercise-induced alterations in oxidative stress and inflammatory processes related to CVDs.

Dr. Anikó Pósa

Dr Renáta Szabó

Guest Editors

Manuscript Submission Information

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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
  • cardiovascular diseases
  • antioxidant therapy
  • physical exercise
  • signaling cascades related to cardiovascular disease (CVD) pathologies.

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Published Papers (3 papers)

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Research

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18 pages, 5435 KiB  
Article
Diabetes Upregulates Oxidative Stress and Downregulates Cardiac Protection to Exacerbate Myocardial Ischemia/Reperfusion Injury in Rats
by Chen-Yen Chien, Ting-Jui Wen, Yu-Hsiuan Cheng, Yi-Ting Tsai, Chih-Yao Chiang and Chiang-Ting Chien
Antioxidants 2020, 9(8), 679; https://0-doi-org.brum.beds.ac.uk/10.3390/antiox9080679 - 29 Jul 2020
Cited by 15 | Viewed by 2773
Abstract
Diabetes exacerbates myocardial ischemia/reperfusion (IR) injury by incompletely understood mechanisms. We explored whether diabetes diminished BAG3/Bcl-2/Nrf-2/HO-1-mediated cardioprotection and overproduced oxidative stress contributing to exaggerated IR injury. Streptozotocin-induced diabetes enhanced hyperglycemia, cardiac NADPH oxidase p22/p67 expression, malondialdehyde amount and leukocyte infiltration, altered the mesenteric [...] Read more.
Diabetes exacerbates myocardial ischemia/reperfusion (IR) injury by incompletely understood mechanisms. We explored whether diabetes diminished BAG3/Bcl-2/Nrf-2/HO-1-mediated cardioprotection and overproduced oxidative stress contributing to exaggerated IR injury. Streptozotocin-induced diabetes enhanced hyperglycemia, cardiac NADPH oxidase p22/p67 expression, malondialdehyde amount and leukocyte infiltration, altered the mesenteric expression of 4-HNE, CaSR, p-eNOS and BAG3 and impaired microvascular reactivity to the vasoconstrictor/vasodilator by a wire myography. In response to myocardial IR, diabetes further depressed BAG3/Bcl-2/Nrf-2/HO-1 expression, increased cleaved-caspase 3/poly(ADP-ribose) polymerase (PARP)/TUNEL-mediated apoptosis and exacerbated IR-induced left ventricular dysfunction characterized by further depressed microcirculation, heart rate, left ventricular systolic pressure and peak rate of pressure increase/decrease (±dp/dt) and elevated left ventricular end-diastolic pressure (LVEDP) and Evans blue-2,3,5-triphenyltetrazolium chloride-stained infarct size in diabetic hearts. Our results implicated diabetes exacerbated IR-induced myocardial dysfunction through downregulated BAG3/Bcl-2/Nrf-2/HO-1 expression, increased p22/p67/caspase 3/PARP/apoptosis-mediated oxidative injury and impaired microvascular reactivity. Full article
(This article belongs to the Special Issue Free Radicals and Cardiovascular Diseases)
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15 pages, 3708 KiB  
Article
MiR155-5p Inhibits Cell Migration and Oxidative Stress in Vascular Smooth Muscle Cells of Spontaneously Hypertensive Rats
by Nan Wu, Chao Ye, Fen Zheng, Guo-Wei Wan, Lu-Lu Wu, Qi Chen, Yue-Hua Li, Yu-Ming Kang and Guo-Qing Zhu
Antioxidants 2020, 9(3), 204; https://0-doi-org.brum.beds.ac.uk/10.3390/antiox9030204 - 01 Mar 2020
Cited by 24 | Viewed by 3657
Abstract
Migration of vascular smooth muscle cells (VSMCs) is essential for vascular reconstruction in hypertension and several vascular diseases. Our recent study showed that extracellular vesicles derived from vascular adventitial fibroblasts of normal rats inhibited VSMC proliferation by delivering miR155-5p to VSMCs. It is [...] Read more.
Migration of vascular smooth muscle cells (VSMCs) is essential for vascular reconstruction in hypertension and several vascular diseases. Our recent study showed that extracellular vesicles derived from vascular adventitial fibroblasts of normal rats inhibited VSMC proliferation by delivering miR155-5p to VSMCs. It is unknown whether miR155-5p inhibits cell migration and oxidative stress in VSMCs of spontaneously hypertensive rats (SHR) and in angiotensin II (Ang II)-treated VSMCs. The purpose of this study was to determine the role of miR155-5p in VSMC migration and its underlying mechanisms. Primary VSMCs were isolated from the aortic media of Wistar-Kyoto rats (WKY) and SHR. Wound healing assay and Boyden chamber assay were used to evaluate VSMC migration. A miR155-5p mimic inhibited, and a miR155-5p inhibitor promoted the migration of VSMC of SHR but had no significant effect on the migration of VSMC of WKY. The miR155-5p mimic inhibited angiotensin-converting enzyme (ACE) mRNA and protein expression in VSMCs. It also reduced superoxide anion production, NAD(P)H oxidase (NOX) activity, as well as NOX2, interleukin-1β (IL-1β), and tumor necrosis factor α (TNF-α) expression levels in VSMCs of SHR but not in VSMCs of WKY rats. Overexpression of miR155-5p inhibited VSMC migration and superoxide anion and IL-1β production in VSMCs of SHR but had no impact on exogenous Ang II-induced VSMC migration and on superoxide anion and IL-1β production in WKY rats and SHR. These results indicate that miR155-5p inhibits VSMC migration in SHR by suppressing ACE expression and its downstream production of Ang II, superoxide anion, and inflammatory factors. However, miR155-5p had no effects on exogenous Ang II-induced VSMC migration. Full article
(This article belongs to the Special Issue Free Radicals and Cardiovascular Diseases)
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Review

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23 pages, 640 KiB  
Review
Vitamin C and Cardiovascular Disease: An Update
by Marco B. Morelli, Jessica Gambardella, Vanessa Castellanos, Valentina Trimarco and Gaetano Santulli
Antioxidants 2020, 9(12), 1227; https://0-doi-org.brum.beds.ac.uk/10.3390/antiox9121227 - 03 Dec 2020
Cited by 73 | Viewed by 14876
Abstract
The potential beneficial effects of the antioxidant properties of vitamin C have been investigated in a number of pathological conditions. In this review, we assess both clinical and preclinical studies evaluating the role of vitamin C in cardiac and vascular disorders, including coronary [...] Read more.
The potential beneficial effects of the antioxidant properties of vitamin C have been investigated in a number of pathological conditions. In this review, we assess both clinical and preclinical studies evaluating the role of vitamin C in cardiac and vascular disorders, including coronary heart disease, heart failure, hypertension, and cerebrovascular diseases. Pitfalls and controversies in investigations on vitamin C and cardiovascular disorders are also discussed. Full article
(This article belongs to the Special Issue Free Radicals and Cardiovascular Diseases)
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