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Antioxidants
Special Issues
Redox and Nitrosative Signaling in Cardioprotection
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Redox and Nitrosative Signaling in Cardioprotection

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 (15 April 2022) | Viewed by 5432

Special Issue Editor

Prof. Dr. Claudia Penna

E-Mail Website
Guest Editor
Laboratory of Cardiovascular Physiology, Dipartimento di Scienze Cliniche e Biologiche, Università Degli Studi di Torino, Regione Gonzole 10, 10043 Orbassano, Italy
Interests: cardiovascular system; physiological endothelial functions; coronary circulation; metabolism; contractility; myocardial protection; endothelial cells; vitamins
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Redox/nitrosative signaling levels are involved in many human physiological adaptations such as physical exercise and in many pathophysiological processes that lead to diseases, such as metabolic syndrome, cancer, neurodegenerative diseases, lung diseases, cardiovascular diseases and ischemic injury/reperfusion. Redox approaches have shown promise in increasing tolerance levels to cardiotoxic anticancer drugs and in protecting or inhibiting the progression of these diseases. The main purpose of this special issue is to reach a large audience of scientists working in the field of redox biomedicine, particularly in regards to cardioprotection. We encourage the submission of articles that address the redox topic from different perspectives and at different levels, from basic to translational research in different biomedical fields. We encourage you to submit your latest research results or review article to this special issue, which will bring together current research on redox and nitrosative signaling in both normal processes and disease states. This research may include both in vitro and in vivo studies related to any of the following topics, but not only to the regulation of antioxidant enzymes; protein-dependent post-translational redox modifications; role of redox states in cell metabolism, cell cycle and cellular communications (eg, extracellular vesicles), epigenetic regulation, cell stress and disease. Studies on organ protection and organ toxicity are also welcome.

We look forward to your contribution.

Prof. Dr. Claudia Penna
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.

Published Papers (2 papers)

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Research

22 pages, 2549 KiB  
Article
The Antioxidant Selenoprotein T Mimetic, PSELT, Induces Preconditioning-like Myocardial Protection by Relieving Endoplasmic-Reticulum Stress
by Carmine Rocca, Anna De Bartolo, Maria Concetta Granieri, Vittoria Rago, Daniela Amelio, Flavia Falbo, Rocco Malivindi, Rosa Mazza, Maria Carmela Cerra, Loubna Boukhzar, Benjamin Lefranc, Jérôme Leprince, Youssef Anouar and Tommaso Angelone
Antioxidants 2022, 11(3), 571; https://doi.org/10.3390/antiox11030571 - 17 Mar 2022
Cited by 9 | Viewed by 2383
Abstract
Oxidative stress and endoplasmic reticulum stress (ERS) are strictly involved in myocardial ischemia/reperfusion (MI/R). Selenoprotein T (SELENOT), a vital thioredoxin-like selenoprotein, is crucial for ER homeostasis and cardiomyocyte differentiation and protection, likely acting as a redox-sensing protein during MI/R. Here, we designed a [...] Read more.
Oxidative stress and endoplasmic reticulum stress (ERS) are strictly involved in myocardial ischemia/reperfusion (MI/R). Selenoprotein T (SELENOT), a vital thioredoxin-like selenoprotein, is crucial for ER homeostasis and cardiomyocyte differentiation and protection, likely acting as a redox-sensing protein during MI/R. Here, we designed a small peptide (PSELT), encompassing the redox site of SELENOT, and investigated whether its pre-conditioning cardioprotective effect resulted from modulating ERS during I/R. The Langendorff rat heart model was employed for hemodynamic analysis, while mechanistic studies were performed in perfused hearts and H9c2 cardiomyoblasts. PSELT improved the post-ischemic contractile recovery, reducing infarct size and LDH release with and without the ERS inducer tunicamycin (TM). Mechanistically, I/R and TM upregulated SELENOT expression, which was further enhanced by PSELT. PSELT also prevented the expression of the ERS markers CHOP and ATF6, reduced cardiac lipid peroxidation and protein oxidation, and increased SOD and catalase activities. An inert PSELT (I-PSELT) lacking selenocysteine was ineffective. In H9c2 cells, H2O2 decreased cell viability and SELENOT expression, while PSELT rescued protein levels protecting against cell death. In SELENOT-deficient H9c2 cells, H2O2 exacerbated cell death, that was partially mitigated by PSELT. Microscopy analysis revealed that a fluorescent form of PSELT was internalized into cardiomyocytes with a perinuclear distribution. Conclusions: The cell-permeable PSELT is able to induce pharmacological preconditioning cardioprotection by mitigating ERS and oxidative stress, and by regulating endogenous SELENOT. Full article
(This article belongs to the Special Issue Redox and Nitrosative Signaling in Cardioprotection)
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18 pages, 5774 KiB  
Article
Dietary Iron Overload and Hfe−/− Related Hemochromatosis Alter Hepatic Mitochondrial Function
by Christine Fischer, Chiara Volani, Timea Komlódi, Markus Seifert, Egon Demetz, Lara Valente de Souza, Kristina Auer, Verena Petzer, Laura von Raffay, Patrizia Moser, Erich Gnaiger and Guenter Weiss
Antioxidants 2021, 10(11), 1818; https://doi.org/10.3390/antiox10111818 - 16 Nov 2021
Cited by 8 | Viewed by 2606
Abstract
Iron is an essential co-factor for many cellular metabolic processes, and mitochondria are main sites of utilization. Iron accumulation promotes production of reactive oxygen species (ROS) via the catalytic activity of iron species. Herein, we investigated the consequences of dietary and genetic iron [...] Read more.
Iron is an essential co-factor for many cellular metabolic processes, and mitochondria are main sites of utilization. Iron accumulation promotes production of reactive oxygen species (ROS) via the catalytic activity of iron species. Herein, we investigated the consequences of dietary and genetic iron overload on mitochondrial function. C57BL/6N wildtype and Hfe−/− mice, the latter a genetic hemochromatosis model, received either normal diet (ND) or high iron diet (HI) for two weeks. Liver mitochondrial respiration was measured using high-resolution respirometry along with analysis of expression of specific proteins and ROS production. HI promoted tissue iron accumulation and slightly affected mitochondrial function in wildtype mice. Hepatic mitochondrial function was impaired in Hfe−/− mice on ND and HI. Compared to wildtype mice, Hfe−/− mice on ND showed increased mitochondrial respiratory capacity. Hfe−/− mice on HI showed very high liver iron levels, decreased mitochondrial respiratory capacity and increased ROS production associated with reduced mitochondrial aconitase activity. Although Hfe−/− resulted in increased mitochondrial iron loading, the concentration of metabolically reactive cytoplasmic iron and mitochondrial density remained unchanged. Our data show multiple effects of dietary and genetic iron loading on mitochondrial function and linked metabolic pathways, providing an explanation for fatigue in iron-overloaded hemochromatosis patients, and suggests iron reduction therapy for improvement of mitochondrial function. Full article
(This article belongs to the Special Issue Redox and Nitrosative Signaling in Cardioprotection)
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