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Antioxidants
Special Issues
Oxidative Stress and Cardiac Turnover Capacity
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Oxidative Stress and Cardiac Turnover Capacity

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 October 2021) | Viewed by 7934

Special Issue Editor

Prof. Dr. Antonio Bernad

E-Mail Website
Guest Editor
Centro Nacional de Biotecnologia (CNB- CSIC), Madrid, Spain
Interests: heart; cardiac progenitor; BMI1; oxidative stress; stemness and cell therapy

Special Issue Information

Dear Colleagues,

Oxidative stress, defined as an imbalance between reactive oxygen species (ROS) production and the endogenous antioxidant defense system, has been demonstrated to be crucial to the onset and progression of many pathophysiological conditions, including cardiovascular disease. The heart is an organ particularly rich in mitochondria, and dysregulation of this large mitochondrial mass alters many signaling pathways crucial to conditioning in numerous cardiac dysfunctions. Apart from cardiomyocytes, an important impact also occurs on other cardiac cell lineages. Although an important body of knowledge is being accumulated on mature cells, less clear evidence exists on the impact of oxidative stress on the capacity of the adult heart to self-repair, especially with regard to resident multipotent progenitors and de-differentiating cardiomyocytes. This is particularly relevant with respect to the aging axis.

We invite you to submit an original research paper or a review article to this Special Issue, which will bring together current research on the impact of oxidative stress on the turnover capacity of the adult heart, both in physiological processes and diseased states. We are particularly interested in in vitro and in vivo studies, in any organism, on any of the following topics:

  • net heart turnover;
  • multipotent resident progenitors;
  • de-differentiation of mature cardiomyocytes;
  • cell metabolism and epigenetic regulation;
  • cellular stress and redox signaling.

We look forward to your contribution.

Prof. Dr. Antonio Bernad
Guest Editor

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

  • ROS
  • oxidative stress
  • redox signaling
  • heart turnover
  • multipotent progenitors
  • de-differentiating cardiomyocytes
  • cell metabolism
  • epigenetic regulation
  • cardiovascular disease
  • aging

Published Papers (3 papers)

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Research

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23 pages, 28660 KiB  
Article
MicroRNA-4732-3p Is Dysregulated in Breast Cancer Patients with Cardiotoxicity, and Its Therapeutic Delivery Protects the Heart from Doxorubicin-Induced Oxidative Stress in Rats
by Rafael Sánchez-Sánchez, Ignacio Reinal, Esteban Peiró-Molina, Marc Buigues, Sandra Tejedor, Amparo Hernándiz, Marta Selva, David Hervás, Antonio J. Cañada, Akaitz Dorronsoro, Ana Santaballa, Carmen Salvador, Florian Caiment, Jos Kleinjans, Luis Martínez-Dolz, Isabel Moscoso, Ricardo Lage, José R. González-Juanatey, Joaquín Panadero, Ernesto Aparicio-Puerta, Antonio Bernad and Pilar Sepúlvedaadd Show full author list remove Hide full author list
Antioxidants 2022, 11(10), 1955; https://doi.org/10.3390/antiox11101955 - 30 Sep 2022
Cited by 7 | Viewed by 2223
Abstract
Anthracycline-induced cardiotoxicity is the most severe collateral effect of chemotherapy originated by an excess of oxidative stress in cardiomyocytes that leads to cardiac dysfunction. We assessed clinical data from patients with breast cancer receiving anthracyclines and searched for discriminating microRNAs between patients that [...] Read more.
Anthracycline-induced cardiotoxicity is the most severe collateral effect of chemotherapy originated by an excess of oxidative stress in cardiomyocytes that leads to cardiac dysfunction. We assessed clinical data from patients with breast cancer receiving anthracyclines and searched for discriminating microRNAs between patients that developed cardiotoxicity (cases) and those that did not (controls), using RNA sequencing and regression analysis. Serum levels of 25 microRNAs were differentially expressed in cases versus controls within the first year after anthracycline treatment, as assessed by three different regression models (elastic net, Robinson and Smyth exact negative binomial test and random forest). MiR-4732-3p was the only microRNA identified in all regression models and was downregulated in patients that experienced cardiotoxicity. MiR-4732-3p was also present in neonatal rat cardiomyocytes and cardiac fibroblasts and was modulated by anthracycline treatment. A miR-4732-3p mimic was cardioprotective in cardiac and fibroblast cultures, following doxorubicin challenge, in terms of cell viability and ROS levels. Notably, administration of the miR-4732-3p mimic in doxorubicin-treated rats preserved cardiac function, normalized weight loss, induced angiogenesis, and decreased apoptosis, interstitial fibrosis and cardiac myofibroblasts. At the molecular level, miR-4732-3p regulated genes of TGFβ and Hippo signaling pathways. Overall, the results indicate that miR-4732-3p is a novel biomarker of cardiotoxicity that has therapeutic potential against anthracycline-induced heart damage. Full article
(This article belongs to the Special Issue Oxidative Stress and Cardiac Turnover Capacity)
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Review

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21 pages, 1213 KiB  
Review
The Vascular Niche for Adult Cardiac Progenitor Cells
by Diego Herrero, Guillermo Albericio, Marina Higuera, María Herranz-López, Miguel A. García-Brenes, Alejandra Cordero, Enrique Roche, Pilar Sepúlveda, Carmen Mora and Antonio Bernad
Antioxidants 2022, 11(5), 882; https://doi.org/10.3390/antiox11050882 - 29 Apr 2022
Cited by 2 | Viewed by 2073
Abstract
Research on cardiac progenitor cell populations has generated expectations about their potential for cardiac regeneration capacity after acute myocardial infarction and during physiological aging; however, the endogenous capacity of the adult mammalian heart is limited. The modest efficacy of exogenous cell-based treatments can [...] Read more.
Research on cardiac progenitor cell populations has generated expectations about their potential for cardiac regeneration capacity after acute myocardial infarction and during physiological aging; however, the endogenous capacity of the adult mammalian heart is limited. The modest efficacy of exogenous cell-based treatments can guide the development of new approaches that, alone or in combination, can be applied to boost clinical efficacy. The identification and manipulation of the adult stem cell environment, termed niche, will be critical for providing new evidence on adult stem cell populations and improving stem-cell-based therapies. Here, we review and discuss the state of our understanding of the interaction of adult cardiac progenitor cells with other cardiac cell populations, with a focus on the description of the B-CPC progenitor population (Bmi1+ cardiac progenitor cell), which is a strong candidate progenitor for all main cardiac cell lineages, both in the steady state and after cardiac damage. The set of all interactions should be able to define the vascular cardiac stem cell niche, which is associated with low oxidative stress domains in vasculature, and whose manipulation would offer new hope in the cardiac regeneration field. Full article
(This article belongs to the Special Issue Oxidative Stress and Cardiac Turnover Capacity)
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14 pages, 1043 KiB  
Review
Unraveling and Targeting Myocardial Regeneration Deficit in Diabetes
by Claudia Molinaro, Luca Salerno, Fabiola Marino, Mariangela Scalise, Nadia Salerno, Loredana Pagano, Antonella De Angelis, Eleonora Cianflone, Daniele Torella and Konrad Urbanek
Antioxidants 2022, 11(2), 208; https://doi.org/10.3390/antiox11020208 - 22 Jan 2022
Cited by 14 | Viewed by 3151
Abstract
Cardiomyopathy is a common complication in diabetic patients. Ventricular dysfunction without coronary atherosclerosis and hypertension is driven by hyperglycemia, hyperinsulinemia and impaired insulin signaling. Cardiomyocyte death, hypertrophy, fibrosis, and cell signaling defects underlie cardiomyopathy. Notably, detrimental effects of the diabetic milieu are not [...] Read more.
Cardiomyopathy is a common complication in diabetic patients. Ventricular dysfunction without coronary atherosclerosis and hypertension is driven by hyperglycemia, hyperinsulinemia and impaired insulin signaling. Cardiomyocyte death, hypertrophy, fibrosis, and cell signaling defects underlie cardiomyopathy. Notably, detrimental effects of the diabetic milieu are not limited to cardiomyocytes and vascular cells. The diabetic heart acquires a senescent phenotype and also suffers from altered cellular homeostasis and the insufficient replacement of dying cells. Chronic inflammation, oxidative stress, and metabolic dysregulation damage the population of endogenous cardiac stem cells, which contribute to myocardial cell turnover and repair after injury. Therefore, deficient myocardial repair and the progressive senescence and dysfunction of stem cells in the diabetic heart can represent potential therapeutic targets. While our knowledge of the effects of diabetes on stem cells is growing, several strategies to preserve, activate or restore cardiac stem cell compartments await to be tested in diabetic cardiomyopathy. Full article
(This article belongs to the Special Issue Oxidative Stress and Cardiac Turnover Capacity)
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