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Antioxidants
Special Issues
Crosstalk Between Oxidative Stress and Inflammation in Cardiovascular Diseases, Cancer...
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Crosstalk Between Oxidative Stress and Inflammation in Cardiovascular Diseases, Cancer and Neurodegeneration

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 (30 November 2023) | Viewed by 6404

Special Issue Editors

Dr. Adrian Manea

E-Mail Website
Guest Editor
Institute of Cellular Biology and Pathology “Nicolae Simionescu” of the Romanian Academy, 050568 Bucharest, Romania
Interests: cardiovascular diseases; atherosclerosis; diabetes; hypertension; redox biology; inflammation; transcriptomics; epigenetics
Dr. Gina Manda

E-Mail Website
Guest Editor
“Victor Babeș” National Institute of Pathology, Splaiul Independentei 99-101, 050096 Bucharest, Romania
Interests: redox biology; NRF2 medicine and therapeutics; immune response; neurodegeneration; cancer; radiotherapy

Special Issue Information

Dear Colleagues,

Extensive evidence demonstrates that many chronic diseases and cancer have a background of chronic low-grade inflammation and redox disturbances that precede the onset of overt symptoms and accompany the disease during its progression. In depth knowledge on the crosstalk of genetic determinants, epigenetic mechanisms and critical transcription factors in inflammation and redox signaling, such as NFkB, AP1 and NRF2, and their interference with various other signaling pathways involved in DNA repair, endoplasmic reticulum stress, autophagy and hypoxia, as well as an integrative analysis of recently generated omics big data, is expected to foster the development of innovative therapeutic strategies for controlling disease in its early stages or as preventive measure for at risk patients. Considering the limitations of the current anti-inflammatory and antioxidant therapies in chronic pathologies, a major research priority is to simultaneously target chronic inflammation and redox disturbances by manipulating signaling pathways, such as the NRF2/KEAP1 axis.

This Special Issue is focused on the current state of the art of preclinical and clinical studies on the inflammation–redox interplay in ageing and related chronic diseases, such as neurodegeneration and cardiovascular, metabolic and immune disorders, as well as in cancer. We invite researchers and clinicians across the globe to submit their contributions (original articles, reviews, systematic reviews, meta-analyses or perspectives relevant to the scope of the Special Issue, including, but not limited to, the following: inflammation; inflammasomes; redox biology; transcription factors; NRF2; epigenetics; aging; cardiovascular pathology; neurodegeneration; macular degeneration; and cancer.

Dr. Adrian Manea
Dr. Gina Manda
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

  • inflammation
  • inflammasomes
  • redox biology
  • transcription factors
  • NRF2
  • epigenetics
  • aging
  • cardiovascular pathology
  • neurodegeneration
  • macular degeneration
  • cancer

Published Papers (4 papers)

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Research

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18 pages, 2456 KiB  
Article
Pyridoxamine Limits Cardiac Dysfunction in a Rat Model of Doxorubicin-Induced Cardiotoxicity
by Sibren Haesen, Manon Marie Jager, Aline Brillouet, Iris de Laat, Lotte Vastmans, Eline Verghote, Anouk Delaet, Sarah D’Haese, Ibrahim Hamad, Markus Kleinewietfeld, Jeroen Mebis, Wilfried Mullens, Ivo Lambrichts, Esther Wolfs, Dorien Deluyker and Virginie Bito
Antioxidants 2024, 13(1), 112; https://doi.org/10.3390/antiox13010112 - 17 Jan 2024
Cited by 1 | Viewed by 1331
Abstract
The use of doxorubicin (DOX) chemotherapy is restricted due to dose-dependent cardiotoxicity. Pyridoxamine (PM) is a vitamin B6 derivative with favorable effects on diverse cardiovascular diseases, suggesting a cardioprotective effect on DOX-induced cardiotoxicity. The cardioprotective nature of PM was investigated in a rat [...] Read more.
The use of doxorubicin (DOX) chemotherapy is restricted due to dose-dependent cardiotoxicity. Pyridoxamine (PM) is a vitamin B6 derivative with favorable effects on diverse cardiovascular diseases, suggesting a cardioprotective effect on DOX-induced cardiotoxicity. The cardioprotective nature of PM was investigated in a rat model of DOX-induced cardiotoxicity. Six-week-old female Sprague Dawley rats were treated intravenously with 2 mg/kg DOX or saline (CTRL) weekly for eight weeks. Two other groups received PM via the drinking water next to DOX (DOX+PM) or saline (CTRL+PM). Echocardiography, strain analysis, and hemodynamic measurements were performed to evaluate cardiac function. Fibrotic remodeling, myocardial inflammation, oxidative stress, apoptosis, and ferroptosis were evaluated by various in vitro techniques. PM significantly attenuated DOX-induced left ventricular (LV) dilated cardiomyopathy and limited TGF-β1-related LV fibrotic remodeling and macrophage-driven myocardial inflammation. PM protected against DOX-induced ferroptosis, as evidenced by restored DOX-induced disturbance of redox balance, improved cytosolic and mitochondrial iron regulation, and reduced mitochondrial damage at the gene level. In conclusion, PM attenuated the development of cardiac damage after DOX treatment by reducing myocardial fibrosis, inflammation, and mitochondrial damage and by restoring redox and iron regulation at the gene level, suggesting that PM may be a novel cardioprotective strategy for DOX-induced cardiomyopathy. Full article
(This article belongs to the Special Issue Crosstalk Between Oxidative Stress and Inflammation in Cardiovascular Diseases, Cancer and Neurodegeneration)
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Review

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27 pages, 3340 KiB  
Review
Crosstalk between Oxidative Stress and Inflammation Caused by Noise and Air Pollution—Implications for Neurodegenerative Diseases
by Marin Kuntić, Omar Hahad, Thomas Münzel and Andreas Daiber
Antioxidants 2024, 13(3), 266; https://doi.org/10.3390/antiox13030266 - 22 Feb 2024
Viewed by 1438
Abstract
Neurodegenerative diseases are often referred to as diseases of old age, and with the aging population, they are gaining scientific and medical interest. Environmental stressors, most notably traffic noise and air pollution, have recently come to the forefront, and have emerged as disease [...] Read more.
Neurodegenerative diseases are often referred to as diseases of old age, and with the aging population, they are gaining scientific and medical interest. Environmental stressors, most notably traffic noise and air pollution, have recently come to the forefront, and have emerged as disease risk factors. The evidence for a connection between environmental risk factors and neurodegenerative disease is growing. In this review, the most common neurodegenerative diseases and their epidemiological association with traffic noise and air pollution are presented. Also, the most important mechanisms involved in neurodegenerative disease development, oxidative stress, and neuroinflammation are highlighted. An overview of the in vivo findings will provide a mechanistic link between noise, air pollution, and neurodegenerative pathology. Finally, the importance of the direct and indirect pathways, by which noise and air pollution cause cerebral damage, is discussed. More high-quality data are still needed from both epidemiological and basic science studies in order to better understand the causal connection between neurodegenerative diseases and environmental risk factors. Full article
(This article belongs to the Special Issue Crosstalk Between Oxidative Stress and Inflammation in Cardiovascular Diseases, Cancer and Neurodegeneration)
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25 pages, 4078 KiB  
Review
The Roles of Neutrophil-Derived Myeloperoxidase (MPO) in Diseases: The New Progress
by Wei Lin, Huili Chen, Xijing Chen and Chaorui Guo
Antioxidants 2024, 13(1), 132; https://doi.org/10.3390/antiox13010132 - 22 Jan 2024
Cited by 2 | Viewed by 1697
Abstract
Myeloperoxidase (MPO) is a heme-containing peroxidase, mainly expressed in neutrophils and, to a lesser extent, in monocytes. MPO is known to have a broad bactericidal ability via catalyzing the reaction of Cl− with H2O2 to produce a strong oxidant, [...] Read more.
Myeloperoxidase (MPO) is a heme-containing peroxidase, mainly expressed in neutrophils and, to a lesser extent, in monocytes. MPO is known to have a broad bactericidal ability via catalyzing the reaction of Cl− with H2O2 to produce a strong oxidant, hypochlorous acid (HOCl). However, the overproduction of MPO-derived oxidants has drawn attention to its detrimental role, especially in diseases characterized by acute or chronic inflammation. Broadly speaking, MPO and its derived oxidants are involved in the pathological processes of diseases mainly through the oxidation of biomolecules, which promotes inflammation and oxidative stress. Meanwhile, some researchers found that MPO deficiency or using MPO inhibitors could attenuate inflammation and tissue injuries. Taken together, MPO might be a promising target for both prognostic and therapeutic interventions. Therefore, understanding the role of MPO in the progress of various diseases is of great value. This review provides a comprehensive analysis of the diverse roles of MPO in the progression of several diseases, including cardiovascular diseases (CVDs), neurodegenerative diseases, cancers, renal diseases, and lung diseases (including COVID-19). This information serves as a valuable reference for subsequent mechanistic research and drug development. Full article
(This article belongs to the Special Issue Crosstalk Between Oxidative Stress and Inflammation in Cardiovascular Diseases, Cancer and Neurodegeneration)
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18 pages, 1158 KiB  
Review
Anti-Inflammation and Anti-Oxidation: The Key to Unlocking the Cardiovascular Potential of SGLT2 Inhibitors and GLP1 Receptor Agonists
by Veronika A. Myasoedova, Michele Bozzi, Vincenza Valerio, Donato Moschetta, Ilaria Massaiu, Valentina Rusconi, Daniele Di Napoli, Michele Ciccarelli, Valentina Parisi, Piergiuseppe Agostoni, Stefano Genovese and Paolo Poggio
Antioxidants 2024, 13(1), 16; https://doi.org/10.3390/antiox13010016 - 20 Dec 2023
Viewed by 1362
Abstract
Type 2 diabetes mellitus (T2DM) is a prevalent and complex metabolic disorder associated with various complications, including cardiovascular diseases. Sodium-glucose co-transporter 2 inhibitors (SGLT2i) and glucagon-like peptide 1 receptor agonists (GLP1-RA) have emerged as novel therapeutic agents for T2DM, primarily aiming to reduce [...] Read more.
Type 2 diabetes mellitus (T2DM) is a prevalent and complex metabolic disorder associated with various complications, including cardiovascular diseases. Sodium-glucose co-transporter 2 inhibitors (SGLT2i) and glucagon-like peptide 1 receptor agonists (GLP1-RA) have emerged as novel therapeutic agents for T2DM, primarily aiming to reduce blood glucose levels. However, recent investigations have unveiled their multifaceted effects, extending beyond their glucose-lowering effect. SGLT2i operate by inhibiting the SGLT2 receptor in the kidneys, facilitating the excretion of glucose through urine, leading to reduced blood glucose levels, while GLP1-RA mimic the action of the GLP1 hormone, stimulating glucose-dependent insulin secretion from pancreatic islets. Both SGLT2i and GLP1-RA have shown remarkable benefits in reducing major cardiovascular events in patients with and without T2DM. This comprehensive review explores the expanding horizons of SGLT2i and GLP1-RA in improving cardiovascular health. It delves into the latest research, highlighting the effects of these drugs on heart physiology and metabolism. By elucidating their diverse mechanisms of action and emerging evidence, this review aims to recapitulate the potential of SGLT2i and GLP1-RA as therapeutic options for cardiovascular health beyond their traditional role in managing T2DM. Full article
(This article belongs to the Special Issue Crosstalk Between Oxidative Stress and Inflammation in Cardiovascular Diseases, Cancer and Neurodegeneration)
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