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Antioxidants
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Implication of Oxidative Stress in Promoting Cell Senescence and Associated...
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Implication of Oxidative Stress in Promoting Cell Senescence and Associated Pathologies

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 May 2023) | Viewed by 13011

Special Issue Editors

Prof. Dr. Dimitrios Galaris

E-Mail Website
Guest Editor
Laboratory of Biological Chemistry, School of Medicine, University of Ioannina, Ioannina, Greece
Interests: mechanisms of oxidative stress-induced cell damage and cell death; oxidative stress and ageing; redox signaling; intracellular labile iron; nutritional iron chelating compounds as antioxidants
Dr. Alexandra Barbouti

E-Mail Website
Guest Editor
Assistant Professor, Laboratory of Anatomy-Histology-Embryology, Faculty of Medicine, University of Ioannina, Ioannina, Greece
Interests: redox signaling; oxidative stress; antioxidants; iron homeostasis; labile iron; apoptotic cell death; cellular senescence
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

It is well known that exposure of several cell types to oxidative stress and reactive oxygen species (ROS) causes a wide range of effects, depending on the intensity and duration of exposure. These effects range from modification of signal transduction pathways and gene expression to an increased rate of cell proliferation, temporary or permanent inhibition of cell proliferation, and finally cell death either caused by apoptosis or necrosis. In the case of permanent inhibition of their proliferation, the cells remain alive but both their phenotype and functional state change dramatically, a condition usually called “cell senescence”.

The presence of increased numbers of senescent cells in tissues is associated with ageing, as well as with several age-associated pathologies such as tissue fibrosis, autoimmune diseases and cancer, among others. Additional knowledge about the molecular mechanisms that underline these interrelationships can lead to new therapeutic approaches for cell senescence-induced ageing and related pathological conditions.

For this Special Issue, we invite researchers to submit original works or review articles related to the implications of oxidative stress in the development of cell senescence, as well as age-related pathologies.

We look forward to receiving your contributions.

Prof. Dr. Dimitrios Galaris
Dr. Alexandra Barbouti
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

  • ageing
  • age-related pathologies
  • cell senescence
  • oxidative stress
  • reactive oxygen species (ROS)

Published Papers (5 papers)

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Research

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26 pages, 3116 KiB  
Article
Oxidative-Stress-Associated Proteostasis Disturbances and Increased DNA Damage in the Hippocampal Granule Cells of the Ts65Dn Model of Down Syndrome
by Alba Puente-Bedia, María T. Berciano, Carmen Martínez-Cué, Miguel Lafarga and Noemí Rueda
Antioxidants 2022, 11(12), 2438; https://doi.org/10.3390/antiox11122438 - 09 Dec 2022
Cited by 4 | Viewed by 1635
Abstract
Oxidative stress (OS) is one of the neuropathological mechanisms responsible for the deficits in cognition and neuronal function in Down syndrome (DS). The Ts65Dn (TS) mouse replicates multiple DS phenotypes including hippocampal-dependent learning and memory deficits and similar brain oxidative status. To better [...] Read more.
Oxidative stress (OS) is one of the neuropathological mechanisms responsible for the deficits in cognition and neuronal function in Down syndrome (DS). The Ts65Dn (TS) mouse replicates multiple DS phenotypes including hippocampal-dependent learning and memory deficits and similar brain oxidative status. To better understand the hippocampal oxidative profile in the adult TS mouse, we analyzed cellular OS-associated alterations in hippocampal granule cells (GCs), a neuronal population that plays an important role in memory formation and that is particularly affected in DS. For this purpose, we used biochemical, molecular, immunohistochemical, and electron microscopy techniques. Our results indicate that TS GCs show important OS-associated alterations in the systems essential for neuronal homeostasis: DNA damage response and proteostasis, particularly of the proteasome and lysosomal system. Specifically, TS GCs showed: (i) increased DNA damage, (ii) reorganization of nuclear proteolytic factories accompanied by a decline in proteasome activity and cytoplasmic aggregation of ubiquitinated proteins, (iii) formation of lysosomal-related structures containing lipid droplets of cytotoxic peroxidation products, and (iv) mitochondrial ultrastructural defects. These alterations could be implicated in enhanced cellular senescence, accelerated aging and neurodegeneration, and the early development of Alzheimer’s disease neuropathology present in TS mice and the DS population. Full article
(This article belongs to the Special Issue Implication of Oxidative Stress in Promoting Cell Senescence and Associated Pathologies)
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Review

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17 pages, 623 KiB  
Review
The Role of Oxidative Stress and Cellular Senescence in the Pathogenesis of Metabolic Associated Fatty Liver Disease and Related Hepatocellular Carcinoma
by Nikolaos-Andreas Anastasopoulos, Antonia V. Charchanti, Alexandra Barbouti, Eleftheria M. Mastoridou, Anna C. Goussia, Anastasia D. Karampa, Dimitrios Christodoulou and Georgios K. Glantzounis
Antioxidants 2023, 12(6), 1269; https://doi.org/10.3390/antiox12061269 - 14 Jun 2023
Cited by 2 | Viewed by 1723
Abstract
Hepatocellular carcinoma (HCC) represents a worryingly increasing cause of malignancy-related mortality, while Metabolic Associated Fatty Liver Disease (MAFLD) is going to become its most common cause in the next decade. Understanding the complex underlying pathophysiology of MAFLD-related HCC can provide opportunities for successful [...] Read more.
Hepatocellular carcinoma (HCC) represents a worryingly increasing cause of malignancy-related mortality, while Metabolic Associated Fatty Liver Disease (MAFLD) is going to become its most common cause in the next decade. Understanding the complex underlying pathophysiology of MAFLD-related HCC can provide opportunities for successful targeted therapies. Of particular interest in this sequela of hepatopathology is cellular senescence, a complex process characterised by cellular cycle arrest initiated by a variety of endogenous and exogenous cell stressors. A key biological process in establishing and maintaining senescence is oxidative stress, which is present in multiple cellular compartments of steatotic hepatocytes. Oxidative stress-induced cellular senescence can change hepatocyte function and metabolism, and alter, in a paracrine manner, the hepatic microenvironment, enabling disease progression from simple steatosis to inflammation and fibrosis, as well as HCC. The duration of senescence and the cell types it affects can tilt the scale from a tumour-protective self-restricting phenotype to the creator of an oncogenic hepatic milieu. A deeper understanding of the mechanism of the disease can guide the selection of the most appropriate senotherapeutic agent, as well as the optimal timing and cell type targeting for effectively combating HCC. Full article
(This article belongs to the Special Issue Implication of Oxidative Stress in Promoting Cell Senescence and Associated Pathologies)
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21 pages, 2127 KiB  
Review
Oxidative Stress-Induced Cellular Senescence: Is Labile Iron the Connecting Link?
by Lambros Nousis, Panagiotis Kanavaros and Alexandra Barbouti
Antioxidants 2023, 12(6), 1250; https://doi.org/10.3390/antiox12061250 - 10 Jun 2023
Cited by 7 | Viewed by 1820
Abstract
Cellular senescence, a cell state characterized by a generally irreversible cell cycle arrest, is implicated in various physiological processes and a wide range of age-related pathologies. Oxidative stress, a condition caused by an imbalance between the production and the elimination of reactive oxygen [...] Read more.
Cellular senescence, a cell state characterized by a generally irreversible cell cycle arrest, is implicated in various physiological processes and a wide range of age-related pathologies. Oxidative stress, a condition caused by an imbalance between the production and the elimination of reactive oxygen species (ROS) in cells and tissues, is a common driver of cellular senescence. ROS encompass free radicals and other molecules formed as byproducts of oxygen metabolism, which exhibit varying chemical reactivity. A prerequisite for the generation of strong oxidizing ROS that can damage macromolecules and impair cellular function is the availability of labile (redox-active) iron, which catalyzes the formation of highly reactive free radicals. Targeting labile iron has been proven an effective strategy to counteract the adverse effects of ROS, but evidence concerning cellular senescence is sparse. In the present review article, we discuss aspects of oxidative stress-induced cellular senescence, with special attention to the potential implication of labile iron. Full article
(This article belongs to the Special Issue Implication of Oxidative Stress in Promoting Cell Senescence and Associated Pathologies)
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18 pages, 1913 KiB  
Review
The Dual Role of Oxidative-Stress-Induced Autophagy in Cellular Senescence: Comprehension and Therapeutic Approaches
by Pavlos Pantelis, George Theocharous, Nefeli Lagopati, Dimitris Veroutis, Dimitris-Foivos Thanos, Giasemi-Panagiota Lampoglou, Natassa Pippa, Maria-Anna Gatou, Ioanna Tremi, Angelos Papaspyropoulos, Efthymios Kyrodimos, Evangelia A. Pavlatou, Maria Gazouli, Konstantinos Evangelou and Vassilis G. Gorgoulis
Antioxidants 2023, 12(1), 169; https://doi.org/10.3390/antiox12010169 - 11 Jan 2023
Cited by 9 | Viewed by 2658
Abstract
The contemporary lifestyle of the last decade has undeniably caused a tremendous increase in oxidative-stress-inducing environmental sources. This phenomenon is not only connected with the rise of ROS levels in multiple tissues but is also associated with the induction of senescence in different [...] Read more.
The contemporary lifestyle of the last decade has undeniably caused a tremendous increase in oxidative-stress-inducing environmental sources. This phenomenon is not only connected with the rise of ROS levels in multiple tissues but is also associated with the induction of senescence in different cell types. Several signaling pathways that are associated with the reduction in ROS levels and the regulation of the cell cycle are being activated, so that the organism can battle deleterious effects. Within this context, autophagy plays a significant role. Through autophagy, cells can maintain their homeostasis, as if it were a self-degradation process, which removes the “wounded” molecules from the cells and uses their materials as a substrate for the creation of new useful cell particles. However, the role of autophagy in senescence has both a “dark” and a “bright” side. This review is an attempt to reveal the mechanistic aspects of this dual role. Nanomedicine can play a significant role, providing materials that are able to act by either preventing ROS generation or controllably inducing it, thus functioning as potential therapeutic agents regulating the activation or inhibition of autophagy. Full article
(This article belongs to the Special Issue Implication of Oxidative Stress in Promoting Cell Senescence and Associated Pathologies)
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21 pages, 3427 KiB  
Review
Oxidative Stress in Age-Related Neurodegenerative Diseases: An Overview of Recent Tools and Findings
by Dimitris Korovesis, Teresa Rubio-Tomás and Nektarios Tavernarakis
Antioxidants 2023, 12(1), 131; https://doi.org/10.3390/antiox12010131 - 05 Jan 2023
Cited by 33 | Viewed by 4284
Abstract
Reactive oxygen species (ROS) have been described to induce a broad range of redox-dependent signaling reactions in physiological conditions. Nevertheless, an excessive accumulation of ROS leads to oxidative stress, which was traditionally considered as detrimental for cells and organisms, due to the oxidative [...] Read more.
Reactive oxygen species (ROS) have been described to induce a broad range of redox-dependent signaling reactions in physiological conditions. Nevertheless, an excessive accumulation of ROS leads to oxidative stress, which was traditionally considered as detrimental for cells and organisms, due to the oxidative damage they cause to biomolecules. During ageing, elevated ROS levels result in the accumulation of damaged proteins, which may exhibit altered enzymatic function or physical properties (e.g., aggregation propensity). Emerging evidence also highlights the relationship between oxidative stress and age-related pathologies, such as protein misfolding-based neurodegenerative diseases (e.g., Parkinson’s (PD), Alzheimer’s (AD) and Huntington’s (HD) diseases). In this review we aim to introduce the role of oxidative stress in physiology and pathology and then focus on the state-of-the-art techniques available to detect and quantify ROS and oxidized proteins in live cells and in vivo, providing a guide to those aiming to characterize the role of oxidative stress in ageing and neurodegenerative diseases. Lastly, we discuss recently published data on the role of oxidative stress in neurological disorders. Full article
(This article belongs to the Special Issue Implication of Oxidative Stress in Promoting Cell Senescence and Associated Pathologies)
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