Search for Articles:
Title / Keyword
Author / Affiliation / Email
Journal
Article Type
 
 
Advanced Search
 
Section
Special Issue
Volume
Issue
Number
Page
 
8.1
4.9
Journals
IJMS
Special Issues
Cellular and Molecular Mechanisms in Oxidative Stress-Related Diseases
ijms-logo
Submit to IJMS Review for IJMS Propose a Special Issue

Journal Menu

► Journal Menu

Journal Browser

► Journal Browser
share announcement

Cellular and Molecular Mechanisms in Oxidative Stress-Related Diseases

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Pathology, Diagnostics, and Therapeutics".

Deadline for manuscript submissions: closed (20 June 2022) | Viewed by 37781

Special Issue Editors

Dr. Rossana Morabito

E-Mail Website
Guest Editor
Department of Chemical, Biological, Pharmaceutical and Environmental Sciences, University of Messina, 98166 Messina, Italy
Interests: physiology; ion trasport; band 3 protein; erythrocytes; oxidative stress; aging
Special Issues, Collections and Topics in MDPI journals
Dr. Alessia Remigante

E-Mail Website
Guest Editor
Department of Chemical, Biological, Pharmaceutical and Environmental Sciences, University of Messina, 98166 Messina, Italy
Interests: human physiology; cell physiology; membrane transport systems; bioactive compound; oxidative stress; human health
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Oxidative stress (OS) is frequently described as the balance between production of reactive species (RS), including oxygen and nitrogen, in biological systems and the ability of the latter to defend through the sophisticated antioxidant machinery. At physiological levels, some oxidants in controlled amounts, possess an important signaling functions within the cell. Specifically, cells can generate RS with function of second messengers, use them for intracellular signaling and for stimulating redox-sensitive signaling pathways to modify the cellular content of the cytoprotective regulatory proteins. In fact, the redox state in the cell is normally regulated by a complex endogenous antioxidant system composed of proteins with enzymatic activity and non-enzymatic proteins able to quickly neutralize or ensure a low production of RS. Nevertheless, when oxidants are produced in excess, or when the antioxidant defenses that regulate them are ineffective, this balance can be perturbed, thus resulting in oxidative condition. Oxidative products are highly reactive, and can directly or indirectly modulate the functions of many enzymes and transcription factors through a complex signaling cascades. In particular, some of the pathways are preferentially linked to enhanced survival, while others are more frequently associated with cell death, and constitute important avenues for therapeutic interventions aimed at limiting oxidative damage or, alternatively, attenuating its consequences. Furthermore, the magnitude and exposure of the insult, as well as the cell type involved are key elements in defining which pathways are activated, as well as the final cell outcome.

The aim of this special issue is to collect and contribute to the dissemination of high quality research articles, as well as review articles, focusing on the relationship between oxidative stress-related diseases and cellular responses in different pathologies, including ischemic stroke, diabetes, kidney disease, cardiovascular and neurodegenerative diseases. In addition, molecular targets of cellular membrane, as well as their potential modulation under oxidative stress will be also considered, in an attempt to provide more information about cell response to oxidative stress and its possible modulation by novel pharmacological strategies.

Prof. Dr. Rossana Morabito
Dr. Alessia Remigante
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. International Journal of Molecular Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. There is an Article Processing Charge (APC) for publication in this open access journal. For details about the APC please see here. 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

  • molecular targets of oxidative stress in oxidative stress related-diseases
  • oxidative stress and oxidative stress-related pathologies
  • cellular response to oxidative stress
  • oxidative stress and apoptosis in oxidative stress-related diseases
  • oxidative stress and related cell signaling
  • cell adaptation to oxidative stress
  • biomarkers of oxidative stress in disease
  • beneficial effects of natural or synthetic antioxidants in oxidative stress-related diseases

Benefits of Publishing in a Special Issue

  • Ease of navigation: Grouping papers by topic helps scholars navigate broad scope journals more efficiently.
  • Greater discoverability: Special Issues support the reach and impact of scientific research. Articles in Special Issues are more discoverable and cited more frequently.
  • Expansion of research network: Special Issues facilitate connections among authors, fostering scientific collaborations.
  • External promotion: Articles in Special Issues are often promoted through the journal's social media, increasing their visibility.
  • e-Book format: Special Issues with more than 10 articles can be published as dedicated e-books, ensuring wide and rapid dissemination.

Further information on MDPI's Special Issue polices can be found here.

Related Special Issue

Published Papers (8 papers)

Download All Papers
Order results
Result details
Show export options expand_more Show export options expand_less
Select all
Export citation of selected articles as:

Editorial

Jump to: Research, Review

4 pages, 191 KiB  
Editorial
Cellular and Molecular Mechanisms in Oxidative Stress-Related Diseases
by Alessia Remigante and Rossana Morabito
Int. J. Mol. Sci. 2022, 23(14), 8017; https://doi.org/10.3390/ijms23148017 - 20 Jul 2022
Cited by 29 | Viewed by 2456
Abstract
The redox equilibrium is important in preserving the correct functionality of vital cellular functions [...] Full article
(This article belongs to the Special Issue Cellular and Molecular Mechanisms in Oxidative Stress-Related Diseases)

Research

Jump to: Editorial, Review

15 pages, 1649 KiB  
Article
Oxidation Stress as a Mechanism of Aging in Human Erythrocytes: Protective Effect of Quercetin
by Alessia Remigante, Sara Spinelli, Nancy Basile, Daniele Caruso, Giuseppe Falliti, Silvia Dossena, Angela Marino and Rossana Morabito
Int. J. Mol. Sci. 2022, 23(14), 7781; https://doi.org/10.3390/ijms23147781 - 14 Jul 2022
Cited by 40 | Viewed by 3238
Abstract
Aging is a multi-factorial process developing through a complex net of interactions between biological and cellular mechanisms and it involves oxidative stress (OS) as well as protein glycation. The aim of the present work was to verify the protective role of Quercetin (Q), [...] Read more.
Aging is a multi-factorial process developing through a complex net of interactions between biological and cellular mechanisms and it involves oxidative stress (OS) as well as protein glycation. The aim of the present work was to verify the protective role of Quercetin (Q), a polyphenolic flavonoid compound, in a d-Galactose (d-Gal)-induced model of aging in human erythrocytes. The anion-exchange capability through the Band 3 protein (B3p) measured by the rate constant of the SO42− uptake, thiobarbituric acid reactive substances (TBARS) levels—a marker of lipid peroxidation—total sulfhydryl (-SH) groups, glycated hemoglobin (A1c), and a reduced glutathione/oxidized glutathione (GSH-GSSG) ratio were determined following the exposure of erythrocytes to 100 mM d-Gal for 24 h, with or without pre-incubation with 10 µM Q. The results confirmed that d-Gal activated OS pathways in human erythrocytes, affecting both membrane lipids and proteins, as denoted by increased TBARS levels and decreased total sulfhydryl groups, respectively. In addition, d-Gal led to an acceleration of the rate constant of the SO42− uptake through the B3p. Both the alteration of the B3p function and oxidative damage have been improved by pre-treatment with Q, which preferentially ameliorated lipid peroxidation rather than protein oxidation. Moreover, Q prevented glycated A1c formation, while no protective effect on the endogenous antioxidant system (GSH-GSSG) was observed. These findings suggest that the B3p could be a novel potential target of antioxidant treatments to counteract aging-related disturbances. Further studies are needed to confirm the possible role of Q in pharmacological strategies against aging. Full article
(This article belongs to the Special Issue Cellular and Molecular Mechanisms in Oxidative Stress-Related Diseases)
►▼ Show Figures

Figure 1

14 pages, 1735 KiB  
Article
Deficiency of AMPKα1 Exacerbates Intestinal Injury and Remote Acute Lung Injury in Mesenteric Ischemia and Reperfusion in Mice
by Hannah V. Hayes, Vivian Wolfe, Michael O’Connor, Nick C. Levinsky, Giovanna Piraino and Basilia Zingarelli
Int. J. Mol. Sci. 2021, 22(18), 9911; https://doi.org/10.3390/ijms22189911 - 14 Sep 2021
Cited by 10 | Viewed by 2619
Abstract
Mesenteric ischemia and reperfusion (I/R) injury can ensue from a variety of vascular diseases and represents a major cause of morbidity and mortality in intensive care units. It causes an inflammatory response associated with local gut dysfunction and remote organ injury. Adenosine monophosphate-activated [...] Read more.
Mesenteric ischemia and reperfusion (I/R) injury can ensue from a variety of vascular diseases and represents a major cause of morbidity and mortality in intensive care units. It causes an inflammatory response associated with local gut dysfunction and remote organ injury. Adenosine monophosphate-activated protein kinase (AMPK) is a crucial regulator of metabolic homeostasis. The catalytic α1 subunit is highly expressed in the intestine and vascular system. In loss-of-function studies, we investigated the biological role of AMPKα1 in affecting the gastrointestinal barrier function. Male knock-out (KO) mice with a systemic deficiency of AMPKα1 and wild-type (WT) mice were subjected to a 30 min occlusion of the superior mesenteric artery. Four hours after reperfusion, AMPKα1 KO mice exhibited exaggerated histological gut injury and impairment of intestinal permeability associated with marked tissue lipid peroxidation and a lower apical expression of the junction proteins occludin and E-cadherin when compared to WT mice. Lung injury with neutrophil sequestration was higher in AMPKα1 KO mice than WT mice and paralleled with higher plasma levels of syndecan-1, a biomarker of endothelial injury. Thus, the data demonstrate that AMPKα1 is an important requisite for epithelial and endothelial integrity and has a protective role in remote organ injury after acute ischemic events. Full article
(This article belongs to the Special Issue Cellular and Molecular Mechanisms in Oxidative Stress-Related Diseases)
►▼ Show Figures

Figure 1

20 pages, 4315 KiB  
Article
TRPM2 Oxidation Activates Two Distinct Potassium Channels in Melanoma Cells through Intracellular Calcium Increase
by Loretta Ferrera, Raffaella Barbieri, Cristiana Picco, Paolo Zuccolini, Alessia Remigante, Sara Bertelli, Maria Rita Fumagalli, Giovanni Zifarelli, Caterina A. M. La Porta, Paola Gavazzo and Michael Pusch
Int. J. Mol. Sci. 2021, 22(16), 8359; https://doi.org/10.3390/ijms22168359 - 4 Aug 2021
Cited by 32 | Viewed by 3078
Abstract
Tumor microenvironments are often characterized by an increase in oxidative stress levels. We studied the response to oxidative stimulation in human primary (IGR39) or metastatic (IGR37) cell lines obtained from the same patient, performing patch-clamp recordings, intracellular calcium ([Ca2+]i) [...] Read more.
Tumor microenvironments are often characterized by an increase in oxidative stress levels. We studied the response to oxidative stimulation in human primary (IGR39) or metastatic (IGR37) cell lines obtained from the same patient, performing patch-clamp recordings, intracellular calcium ([Ca2+]i) imaging, and RT-qPCR gene expression analysis. In IGR39 cells, chloramine-T (Chl-T) activated large K+ currents (KROS) that were partially sensitive to tetraethylammonium (TEA). A large fraction of KROS was inhibited by paxilline—a specific inhibitor of large-conductance Ca2+-activated BK channels. The TEA-insensitive component was inhibited by senicapoc—a specific inhibitor of the Ca2+-activated KCa3.1 channel. Both BK and KCa3.1 activation were mediated by an increase in [Ca2+]i induced by Chl-T. Both KROS and [Ca2+]i increase were inhibited by ACA and clotrimazole—two different inhibitors of the calcium-permeable TRPM2 channel. Surprisingly, IGR37 cells did not exhibit current increase upon the application of Chl-T. Expression analysis confirmed that the genes encoding BK, KCa3.1, and TRPM2 are much more expressed in IGR39 than in IGR37. The potassium currents and [Ca2+]i increase observed in response to the oxidizing agent strongly suggest that these three molecular entities play a major role in the progression of melanoma. Pharmacological targeting of either of these ion channels could be a new strategy to reduce the metastatic potential of melanoma cells, and could complement classical radio- or chemotherapeutic treatments. Full article
(This article belongs to the Special Issue Cellular and Molecular Mechanisms in Oxidative Stress-Related Diseases)
►▼ Show Figures

Figure 1

Review

Jump to: Editorial, Research

22 pages, 2577 KiB  
Review
Cellular and Molecular Signatures of Oxidative Stress in Bronchial Epithelial Cell Models Injured by Cigarette Smoke Extract
by Chiara Cipollina, Andreina Bruno, Salvatore Fasola, Marta Cristaldi, Bernardo Patella, Rosalinda Inguanta, Antonio Vilasi, Giuseppe Aiello, Stefania La Grutta, Claudia Torino and Elisabetta Pace
Int. J. Mol. Sci. 2022, 23(3), 1770; https://doi.org/10.3390/ijms23031770 - 4 Feb 2022
Cited by 30 | Viewed by 4091
Abstract
Exposure of the airways epithelium to environmental insults, including cigarette smoke, results in increased oxidative stress due to unbalance between oxidants and antioxidants in favor of oxidants. Oxidative stress is a feature of inflammation and promotes the progression of chronic lung diseases, including [...] Read more.
Exposure of the airways epithelium to environmental insults, including cigarette smoke, results in increased oxidative stress due to unbalance between oxidants and antioxidants in favor of oxidants. Oxidative stress is a feature of inflammation and promotes the progression of chronic lung diseases, including Chronic Obstructive Pulmonary Disease (COPD). Increased oxidative stress leads to exhaustion of antioxidant defenses, alterations in autophagy/mitophagy and cell survival regulatory mechanisms, thus promoting cell senescence. All these events are amplified by the increase of inflammation driven by oxidative stress. Several models of bronchial epithelial cells are used to study the molecular mechanisms and the cellular functions altered by cigarette smoke extract (CSE) exposure, and to test the efficacy of molecules with antioxidant properties. This review offers a comprehensive synthesis of human in-vitro and ex-vivo studies published from 2011 to 2021 describing the molecular and cellular mechanisms evoked by CSE exposure in bronchial epithelial cells, the most used experimental models and the mechanisms of action of cellular antioxidants systems as well as natural and synthetic antioxidant compounds. Full article
(This article belongs to the Special Issue Cellular and Molecular Mechanisms in Oxidative Stress-Related Diseases)
►▼ Show Figures

Figure 1

26 pages, 12924 KiB  
Review
The Pathomechanism, Antioxidant Biomarkers, and Treatment of Oxidative Stress-Related Eye Diseases
by Yi-Jen Hsueh, Yen-Ning Chen, Yu-Ting Tsao, Chao-Min Cheng, Wei-Chi Wu and Hung-Chi Chen
Int. J. Mol. Sci. 2022, 23(3), 1255; https://doi.org/10.3390/ijms23031255 - 23 Jan 2022
Cited by 80 | Viewed by 9294
Abstract
Oxidative stress is an important pathomechanism found in numerous ocular degenerative diseases. To provide a better understanding of the mechanism and treatment of oxidant/antioxidant imbalance-induced ocular diseases, this article summarizes and provides updates on the relevant research. We review the oxidative damage (e.g., [...] Read more.
Oxidative stress is an important pathomechanism found in numerous ocular degenerative diseases. To provide a better understanding of the mechanism and treatment of oxidant/antioxidant imbalance-induced ocular diseases, this article summarizes and provides updates on the relevant research. We review the oxidative damage (e.g., lipid peroxidation, DNA lesions, autophagy, and apoptosis) that occurs in different areas of the eye (e.g., cornea, anterior chamber, lens, retina, and optic nerve). We then introduce the antioxidant mechanisms present in the eye, as well as the ocular diseases that occur as a result of antioxidant imbalances (e.g., keratoconus, cataracts, age-related macular degeneration, and glaucoma), the relevant antioxidant biomarkers, and the potential of predictive diagnostics. Finally, we discuss natural antioxidant therapies for oxidative stress-related ocular diseases. Full article
(This article belongs to the Special Issue Cellular and Molecular Mechanisms in Oxidative Stress-Related Diseases)
►▼ Show Figures

Graphical abstract

24 pages, 1369 KiB  
Review
Crosstalk between Oxidative Stress and Inflammatory Liver Injury in the Pathogenesis of Alcoholic Liver Disease
by Yoon Mee Yang, Ye Eun Cho and Seonghwan Hwang
Int. J. Mol. Sci. 2022, 23(2), 774; https://doi.org/10.3390/ijms23020774 - 11 Jan 2022
Cited by 108 | Viewed by 7005
Abstract
Alcoholic liver disease (ALD) is characterized by the injury, inflammation, and scarring in the liver owing to excessive alcohol consumption. Currently, ALD is a leading cause for liver transplantation. Therefore, extensive studies (in vitro, in experimental ALD models and in humans) are needed [...] Read more.
Alcoholic liver disease (ALD) is characterized by the injury, inflammation, and scarring in the liver owing to excessive alcohol consumption. Currently, ALD is a leading cause for liver transplantation. Therefore, extensive studies (in vitro, in experimental ALD models and in humans) are needed to elucidate pathological features and pathogenic mechanisms underlying ALD. Notably, oxidative changes in the liver have been recognized as a signature trait of ALD. Progression of ALD is linked to the generation of highly reactive free radicals by reactions involving ethanol and its metabolites. Furthermore, hepatic oxidative stress promotes tissue injury and, in turn, stimulates inflammatory responses in the liver, forming a pathological loop that promotes the progression of ALD. Accordingly, accumulating further knowledge on the relationship between oxidative stress and inflammation may help establish a viable therapeutic approach for treating ALD. Full article
(This article belongs to the Special Issue Cellular and Molecular Mechanisms in Oxidative Stress-Related Diseases)
►▼ Show Figures

Figure 1

15 pages, 4036 KiB  
Review
Correlation between Oxidative Stress and Transforming Growth Factor-Beta in Cancers
by Jinwook Chung, Md Nazmul Huda, Yoonhwa Shin, Sunhee Han, Salima Akter, Insug Kang, Joohun Ha, Wonchae Choe, Tae Gyu Choi and Sung Soo Kim
Int. J. Mol. Sci. 2021, 22(24), 13181; https://doi.org/10.3390/ijms222413181 - 7 Dec 2021
Cited by 26 | Viewed by 4008
Abstract
The downregulation of reactive oxygen species (ROS) facilitates precancerous tumor development, even though increasing the level of ROS can promote metastasis. The transforming growth factor-beta (TGF-β) signaling pathway plays an anti-tumorigenic role in the initial stages of cancer development but a pro-tumorigenic role [...] Read more.
The downregulation of reactive oxygen species (ROS) facilitates precancerous tumor development, even though increasing the level of ROS can promote metastasis. The transforming growth factor-beta (TGF-β) signaling pathway plays an anti-tumorigenic role in the initial stages of cancer development but a pro-tumorigenic role in later stages that fosters cancer metastasis. TGF-β can regulate the production of ROS unambiguously or downregulate antioxidant systems. ROS can influence TGF-β signaling by enhancing its expression and activation. Thus, TGF-β signaling and ROS might significantly coordinate cellular processes that cancer cells employ to expedite their malignancy. In cancer cells, interplay between oxidative stress and TGF-β is critical for tumorigenesis and cancer progression. Thus, both TGF-β and ROS can develop a robust relationship in cancer cells to augment their malignancy. This review focuses on the appropriate interpretation of this crosstalk between TGF-β and oxidative stress in cancer, exposing new potential approaches in cancer biology. Full article
(This article belongs to the Special Issue Cellular and Molecular Mechanisms in Oxidative Stress-Related Diseases)
►▼ Show Figures

Figure 1

Show export options expand_more Show export options expand_less
Select all
Export citation of selected articles as:
 
Displaying articles 1-8
Back to TopTop