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Antioxidants
Special Issues
Mitochondrial Redox in Cardio-Metabolic Disease and Cardio-Oncology
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Mitochondrial Redox in Cardio-Metabolic Disease and Cardio-Oncology

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 (10 February 2022) | Viewed by 4376

Special Issue Editors

Dr. Aaron Sverdlov

E-Mail Website1 Website2
Guest Editor
1. School of Medicine and Public Health, College of Health, Medicine and Wellbeing, University of Newcastle, Callaghan, NSW, Australia
2. Hunter Medical Research Institute, New Lambton Heights, Australia
Interests: cardio-oncology; cardiometabolic; obesity; heart failure; redox stress; biomarkers; general cardiology
Special Issues, Collections and Topics in MDPI journals
Dr. Doan Ngo

E-Mail Website1 Website2
Guest Editor
1. School of Biomedical Sciences and Pharmacy, College of Health, Medicine and Wellbeing, University of Newcastle, Callaghan, NSW, Australia
2. Hunter Medical Research Institute, New Lambton Heights, Australia
Interests: cardio-oncology; cardiometabolic; obesity; heart failure; redox stress; biomarkers; vascular biology
Special Issues, Collections and Topics in MDPI journals
Prof. Dr. Gemma Figtree

E-Mail Website
Guest Editor
Northern Clinical School, Kolling Institute of Medical Research, Faculty of Medicine and Health, St Leonards, Australia
Interests: coronary atherosclerosis; inflammation and oxidative stress in the heart and blood vessel; Clinical trials
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Increased oxidative stress has emerged as a major mediator of pathophysiological processes in many cardiovascular disease states, as well as major cardiovascular risk factors including obesity, cardiometabolic syndrome, and diabetes. Cardio-oncology, a new subspecialty concerned with cardiovascular complications of cancer and cancer therapies, is an emerging and rapidly growing area clinical concern and expanding research direction. Oxidative stress has also been proposed to play an important role in some of the toxicities of anticancer therapies.

While cellular oxidases are known sources of reactive oxygen species, mitochondria has now been implicated as a major source of reactive oxygen species, especially in diabetes, obesity, and cardiovascular diseases. Furthermore, oxidative-stress-mediated mitochondrial dysfunction has emerged as a potential key mechanism behind a number of cardiovascular diseases. It has also been postulated to be the driver of anthracycline-mediated cardiotoxicity and involved in other cancer-therapy-associated cardiovascular toxicities.

We invite original research and review articles focusing on role of mitochondrial oxidative stress in the setting of cardiometabolic disease and cardio-oncology.

Dr. Aaron Sverdlov
Dr. Doan Ngo
Prof. Dr. Gemma Figtree
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

  • Mitochondrial oxidative stress 
  • Cardiometabolic syndrome 
  • Cardio-oncology 
  • Oxidative posttranslational modifications of proteins 
  • Redox therapeutics in cardiovascular disease 
  • Biomarkers of cardiovascular oxidative stress

Published Papers (1 paper)

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Research

17 pages, 2151 KiB  
Article
Patient Endothelial Colony-Forming Cells to Model Coronary Artery Disease Susceptibility and Unravel the Role of Dysregulated Mitochondrial Redox Signalling
by Marie Besnier, Meghan Finemore, Christine Yu, Katharine A. Kott, Stephen T. Vernon, Nicole A. Seebacher, Elijah Genetzakis, Anamarija Furman, Owen Tang, Ryan L. Davis, Thomas Hansen, Peter J. Psaltis, Kristen J. Bubb, Steven G. Wise, Stuart M. Grieve, Belinda A. Di Bartolo and Gemma A. Figtree
Antioxidants 2021, 10(10), 1547; https://0-doi-org.brum.beds.ac.uk/10.3390/antiox10101547 - 29 Sep 2021
Cited by 7 | Viewed by 3220
Abstract
Mechanisms involved in the individual susceptibility to atherosclerotic coronary artery disease (CAD) beyond traditional risk factors are poorly understood. Here, we describe the utility of cultured patient-derived endothelial colony-forming cells (ECFCs) in examining novel mechanisms of CAD susceptibility, particularly the role of dysregulated [...] Read more.
Mechanisms involved in the individual susceptibility to atherosclerotic coronary artery disease (CAD) beyond traditional risk factors are poorly understood. Here, we describe the utility of cultured patient-derived endothelial colony-forming cells (ECFCs) in examining novel mechanisms of CAD susceptibility, particularly the role of dysregulated redox signalling. ECFCs were selectively cultured from peripheral blood mononuclear cells from 828 patients from the BioHEART-CT cohort, each with corresponding demographic, clinical and CT coronary angiographic imaging data. Spontaneous growth occurred in 178 (21.5%) patients and was more common in patients with hypertension (OR 1.45 (95% CI 1.03–2.02), p = 0.031), and less likely in patients with obesity (OR 0.62 [95% CI 0.40–0.95], p = 0.027) or obstructive CAD (stenosis > 50%) (OR 0.60 [95% CI 0.38–0.95], p = 0.027). ECFCs from patients with CAD had higher mitochondrial production of superoxide (O2−–MitoSOX assay). The latter was strongly correlated with the severity of CAD as measured by either coronary artery calcium score (R2 = 0.46; p = 0.0051) or Gensini Score (R2 = 0.67; p = 0.0002). Patient-derived ECFCs were successfully cultured in 3D culture pulsatile mini-vessels. Patient-derived ECFCs can provide a novel resource for discovering mechanisms of CAD disease susceptibility, particularly in relation to mitochondrial redox signalling. Full article
(This article belongs to the Special Issue Mitochondrial Redox in Cardio-Metabolic Disease and Cardio-Oncology)
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