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Biomedicines
Special Issues
The Reactive Oxygen Species Signaling Pathway: Function and Regulation
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The Reactive Oxygen Species Signaling Pathway: Function and Regulation

A special issue of Biomedicines (ISSN 2227-9059). This special issue belongs to the section "Cell Biology and Pathology".

Deadline for manuscript submissions: closed (31 March 2024) | Viewed by 4421

Special Issue Editors

Dr. Tiziana Genovese

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Guest Editor
Department of Chemical, Biological, Pharmaceutical and Environmental Science, University of Messina, 98122 Messina, Italy
Interests: antioxidant; anti-inflammatory
Special Issues, Collections and Topics in MDPI journals
Dr. Daniela Impellizzeri

E-Mail Website
Guest Editor
Department of Chemical, Biological, Pharmaceutical and Environmental Sciences, University of Messina, Via F. Stagno D’Alcontres 31, 98166 Messina, Italy
Interests: inflammation; oxidative stress; biochemistry; pharmacology; molecular biology
Special Issues, Collections and Topics in MDPI journals
Dr. Rosalba Siracusa

E-Mail Website
Guest Editor
Department of Chemical, Biological, Pharmaceutical and Environmental Science, University of Messina, 98122 Messina, Italy
Interests: clinical biochemistry; molecular biology; biomarkers
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

The ability of reactive oxygen species (ROS) to activate or deactivate a variety of receptors, proteins, ions, and other signaling molecules (NF-kB, MAPK, Keap1-Nrf2-ARE, and PI3K-Akt) has made it abundantly clear that redox balance plays a critical role in the physiological and pathological events of cells. When the redox balance is disrupted because of excessive accumulation or depletion of ROS, many cellular signaling pathways are affected, resulting in cellular dysfunction and the development of various pathologies such as cardiovascular, metabolic, neurodegenerative, and inflammatory pathologies, as well as those related to aging. The endogenous antioxidant response system, which is mediated by the transcription factor Nrf2, shields cells from oxidative stress by boosting the production of cytoprotective enzymes. Nrf2 has been proven to have anti-inflammatory effects as well as an influence on mitochondrial activity and biogenesis, in addition to controlling the expression of antioxidant genes. This signal is only one of several defense mechanisms that our bodies might activate to slow the progression of neurodegenerative disorders.

This Special Issue will focus on potential novel treatment targets for inflammatory and neurodegenerative disorders. Its goal will be to identify antioxidant system activators that can be employed as medicinal agents. The Special Issue will include reviews, as well as original in vivo, in vitro, and preclinical research, that demonstrate the therapeutic impacts of novel molecules or natural compounds.

Dr. Tiziana Genovese
Dr. Daniela Impellizzeri
Dr. Rosalba Siracusa
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. Biomedicines 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 2600 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
  • antioxidant systems
  • natural compounds
  • novel molecules
  • human health

Published Papers (3 papers)

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Review

20 pages, 647 KiB  
Review
Cutaneous Redox Senescence
by Mariáurea Matias Sarandy, Reggiani Vilela Gonçalves and Giuseppe Valacchi
Biomedicines 2024, 12(2), 348; https://doi.org/10.3390/biomedicines12020348 - 01 Feb 2024
Viewed by 1153
Abstract
Our current understanding of skin cell senescence involves the role of environmental stressors (UV, O3, cigarette smoke, particulate matter, etc.), lifestyle (diet, exercise, etc.) as well as genetic factors (metabolic changes, hormonal, etc.). The common mechanism of action of these stressors [...] Read more.
Our current understanding of skin cell senescence involves the role of environmental stressors (UV, O3, cigarette smoke, particulate matter, etc.), lifestyle (diet, exercise, etc.) as well as genetic factors (metabolic changes, hormonal, etc.). The common mechanism of action of these stressors is the disturbance of cellular redox balance characterized by increased free radicals and reactive oxygen species (ROS), and when these overload the intrinsic antioxidant defense system, it can lead to an oxidative stress cellular condition. The main redox mechanisms that activate cellular senescence in the skin involve (1) the oxidative damage of telomeres causing their shortening; (2) the oxidation of proteomes and DNA damage; (3) an a in lysosomal mass through the increased activity of resident enzymes such as senescence-associated β-galactosidase (SA-β-gal) as well as other proteins that are products of lysosomal activity; (4) and the increased expression of SASP, in particular pro-inflammatory cytokines transcriptionally regulated by NF-κB. However, the main targets of ROS on the skin are the proteome (oxi-proteome), followed by telomeres, nucleic acids (DNAs), lipids, proteins, and cytoplasmic organelles. As a result, cell cycle arrest pathways, lipid peroxidation, increased lysosomal content and dysfunctional mitochondria, and SASP synthesis occur. Furthermore, oxidative stress in skin cells increases the activity of p16INK4A and p53 as inhibitors of Rb and CDks, which are important for maintaining the cell cycle. p53 also promotes the inactivation of mTOR-mediated autophagic and apoptotic pathways, leading to senescence. However, these markers alone cannot establish the state of cellular senescence, and multiple analyses are encouraged for confirmation. An updated and more comprehensive approach to investigating skin senescence should include further assays of ox-inflammatory molecular pathways that can consolidate the understanding of cutaneous redox senescence. Full article
(This article belongs to the Special Issue The Reactive Oxygen Species Signaling Pathway: Function and Regulation)
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16 pages, 2691 KiB  
Review
Oxidative Stress and the Pathogenesis of Aortic Aneurysms
by Matthew Kazaleh, Rachel Gioscia-Ryan, Gorav Ailawadi and Morgan Salmon
Biomedicines 2024, 12(1), 3; https://doi.org/10.3390/biomedicines12010003 - 19 Dec 2023
Cited by 1 | Viewed by 919
Abstract
Aortic aneurysms are responsible for significant morbidity and mortality. Despite their clinical significance, there remain critical knowledge gaps in the pathogenesis of aneurysm disease and the mechanisms involved in aortic rupture. Recent studies have drawn attention to the role of reactive oxygen species [...] Read more.
Aortic aneurysms are responsible for significant morbidity and mortality. Despite their clinical significance, there remain critical knowledge gaps in the pathogenesis of aneurysm disease and the mechanisms involved in aortic rupture. Recent studies have drawn attention to the role of reactive oxygen species (ROS) and their down-stream effectors in chronic cardiovascular diseases and specifically in the pathogenesis of aortic aneurysm formation. This review will discuss current mechanisms of ROS in mediating aortic aneurysms, the failure of endogenous antioxidant systems in chronic vascular diseases, and their relation to the development of aortic aneurysms. Full article
(This article belongs to the Special Issue The Reactive Oxygen Species Signaling Pathway: Function and Regulation)
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17 pages, 1976 KiB  
Review
Oxidative Stress in Health and Disease
by V. Prakash Reddy
Biomedicines 2023, 11(11), 2925; https://doi.org/10.3390/biomedicines11112925 - 29 Oct 2023
Cited by 7 | Viewed by 1809
Abstract
Oxidative stress, resulting from the excessive intracellular accumulation of reactive oxygen species (ROS), reactive nitrogen species (RNS), and other free radical species, contributes to the onset and progression of various diseases, including diabetes, obesity, diabetic nephropathy, diabetic neuropathy, and neurological diseases, such as [...] Read more.
Oxidative stress, resulting from the excessive intracellular accumulation of reactive oxygen species (ROS), reactive nitrogen species (RNS), and other free radical species, contributes to the onset and progression of various diseases, including diabetes, obesity, diabetic nephropathy, diabetic neuropathy, and neurological diseases, such as Alzheimer’s disease (AD), amyotrophic lateral sclerosis (ALS), and Parkinson’s disease (PD). Oxidative stress is also implicated in cardiovascular disease and cancer. Exacerbated oxidative stress leads to the accelerated formation of advanced glycation end products (AGEs), a complex mixture of crosslinked proteins and protein modifications. Relatively high levels of AGEs are generated in diabetes, obesity, AD, and other I neurological diseases. AGEs such as Ne-carboxymethyllysine (CML) serve as markers for disease progression. AGEs, through interaction with receptors for advanced glycation end products (RAGE), initiate a cascade of deleterious signaling events to form inflammatory cytokines, and thereby further exacerbate oxidative stress in a vicious cycle. AGE inhibitors, AGE breakers, and RAGE inhibitors are therefore potential therapeutic agents for multiple diseases, including diabetes and AD. The complexity of the AGEs and the lack of well-established mechanisms for AGE formation are largely responsible for the lack of effective therapeutics targeting oxidative stress and AGE-related diseases. This review addresses the role of oxidative stress in the pathogenesis of AGE-related chronic diseases, including diabetes and neurological disorders, and recent progress in the development of therapeutics based on antioxidants, AGE breakers and RAGE inhibitors. Furthermore, this review outlines therapeutic strategies based on single-atom nanozymes that attenuate oxidative stress through the sequestering of reactive oxygen species (ROS) and reactive nitrogen species (RNS). Full article
(This article belongs to the Special Issue The Reactive Oxygen Species Signaling Pathway: Function and Regulation)
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