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Biomolecules
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New Insights into Reactive Oxygen Species in Cell Death and...
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New Insights into Reactive Oxygen Species in Cell Death and Immunity

A special issue of Biomolecules (ISSN 2218-273X). This special issue belongs to the section "Cellular Biochemistry".

Deadline for manuscript submissions: closed (30 November 2024) | Viewed by 11957

Special Issue Editors

Dr. Nades Palaniyar

E-Mail Website
Guest Editor
Program in Translational Medicine, PGCRL, The Hospital for Sick Children, and Dept. of Lab Medicine and Pathobiology, and the Institute of Medical Sciences, Faculty of Medicine, University of Toronto, Toronto, ON, Canada
Interests: AI in medicine; infectious and inflammatory diseases; neutrophil extracellular traps (NETs); molecualr mechanisms; drug scrreening
Special Issues, Collections and Topics in MDPI journals
Dr. Marko Radic

E-Mail Website
Guest Editor
Department of Microbiology, Immunology and Biochemistry, College of Medicine, The University of Tennessee Health Science Center, Memphis, TN 38163, USA
Interests: autoantibodies; autoimmunity; B cell development; chimeric antigen receptors (CARs); cytotoxic T cells; histones; neutrophils; post-translational modifications
Special Issues, Collections and Topics in MDPI journals
Dr. Dhia Azzouz

E-Mail Website
Guest Editor
Department of Laboratory Medicine and Pathobiology, University of Toronto, Toronto, ON, Canada
Interests: reactive oxygen species (ROS); NET formation; molecular mechanisms; kinases; mitochondria; a unified model of NET formation; lipid mediators; apoptosis during NET formation; pH; iPS-derived neutrophils; inflammatory lung diseases sepsis; cystic fibrosis; rare lung diseases; innate immune proteins; complement; drugs for regulating NET formation

Special Issue Information

Dear Colleagues,

You are invited to contribute to a Special Issue of Biomolecules entitled “New Insights into Reactive Oxygen Species (ROS) in Cell Death and Immunity”. This Issue aims to assemble a comprehensive collection of research and review articles focusing on ROS (e.g., superoxide anion, hydrogen peroxide, hydroxyl radical, singlet oxygen, peroxynitrite, hypochlorous acid, and others) in cell death pathways (e.g., apoptosis, autophagy, mitophagy, pyroptosis, necrosis, necroptosis, NETosis, METosis, ETosis, and others) and immune response.

This Issue will cover topics including, but not limited to, understanding the role of ROS in infection, inflammation, autoimmunity, metabolic dysregulation, tissue damage, aging and other disorders (e.g., diabetes, obesity, genetic, rare, cancer, lung, kidney, cardiovascular and other diseases), as well as investigating therapeutic targets and strategies for ROS regulation (e.g., drugs).

We also welcome papers that focus on ROS-modulating organelles (e.g., mitochondria, peroxisomes, endoplasmic reticulum, nucleus, lysosomes, plasma membrane, and others), ROS-modulating enzymes (e.g., superoxide dismutase, catalase, glutathione peroxidase, peroxiredoxins, glutathione reductase, NADPH oxidases, mitochondrial electron transport chain enzymes, and others), the interplay between ROS and other reactive molecules (e.g., nitric oxide, nitrogen dioxide, nitrous oxide, nitryl chloride and others), techniques to detect ROS, and models to study ROS in vivo and in vitro.

A given paper could focus on more than one of the topics outlined above.

Dr. Nades Palaniyar
Dr. Marko Radic
Dr. Dhia Azzouz
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. Biomolecules 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 2700 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

  • reactive oxygen species (ROS)
  • cell death
  • immune response
  • ROS-mediated diseases
  • tools to study ROS

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

Published Papers (3 papers)

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Research

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16 pages, 4359 KiB  
Article
Neutrophil Activity and Extracellular Matrix Degradation: Drivers of Lung Tissue Destruction in Fatal COVID-19 Cases and Implications for Long COVID
by Teluguakula Narasaraju, Indira Neeli, Sheila L. Criswell, Amita Krishnappa, Wenzhao Meng, Vasuki Silva, Galyna Bila, Volodymyr Vovk, Zolotukhin Serhiy, Gary L. Bowlin, Nuala Meyer, Eline T. Luning Prak, Marko Radic and Rostyslav Bilyy
Biomolecules 2024, 14(2), 236; https://doi.org/10.3390/biom14020236 - 17 Feb 2024
Cited by 5 | Viewed by 3475
Abstract
Pulmonary fibrosis, severe alveolitis, and the inability to restore alveolar epithelial architecture are primary causes of respiratory failure in fatal COVID-19 cases. However, the factors contributing to abnormal fibrosis in critically ill COVID-19 patients remain unclear. This study analyzed the histopathology of lung [...] Read more.
Pulmonary fibrosis, severe alveolitis, and the inability to restore alveolar epithelial architecture are primary causes of respiratory failure in fatal COVID-19 cases. However, the factors contributing to abnormal fibrosis in critically ill COVID-19 patients remain unclear. This study analyzed the histopathology of lung specimens from eight COVID-19 and six non-COVID-19 postmortems. We assessed the distribution and changes in extracellular matrix (ECM) proteins, including elastin and collagen, in lung alveoli through morphometric analyses. Our findings reveal the significant degradation of elastin fibers along the thin alveolar walls of the lung parenchyma, a process that precedes the onset of interstitial collagen deposition and widespread intra-alveolar fibrosis. Lungs with collapsed alveoli and organized fibrotic regions showed extensive fragmentation of elastin fibers, accompanied by alveolar epithelial cell death. Immunoblotting of lung autopsy tissue extracts confirmed elastin degradation. Importantly, we found that the loss of elastin was strongly correlated with the induction of neutrophil elastase (NE), a potent protease that degrades ECM. This study affirms the critical role of neutrophils and neutrophil enzymes in the pathogenesis of COVID-19. Consistently, we observed increased staining for peptidyl arginine deiminase, a marker for neutrophil extracellular trap release, and myeloperoxidase, an enzyme-generating reactive oxygen radical, indicating active neutrophil involvement in lung pathology. These findings place neutrophils and elastin degradation at the center of impaired alveolar function and argue that elastolysis and alveolitis trigger abnormal ECM repair and fibrosis in fatal COVID-19 cases. Importantly, this study has implications for severe COVID-19 complications, including long COVID and other chronic inflammatory and fibrotic disorders. Full article
(This article belongs to the Special Issue New Insights into Reactive Oxygen Species in Cell Death and Immunity)
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Review

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25 pages, 4216 KiB  
Review
Mitophagy in Cell Death Regulation: Insights into Mechanisms and Disease Implications
by Jiani Lin, Xinyao Chen, Yuyang Du, Jiapeng Li, Tingting Guo and Sai Luo
Biomolecules 2024, 14(10), 1270; https://doi.org/10.3390/biom14101270 - 9 Oct 2024
Cited by 2 | Viewed by 5057
Abstract
Mitophagy, a selective form of autophagy, plays a crucial role in maintaining optimal mitochondrial populations, normal function, and intracellular homeostasis by monitoring and removing damaged or excess mitochondria. Furthermore, mitophagy promotes mitochondrial degradation via the lysosomal pathway, and not only eliminates damaged mitochondria [...] Read more.
Mitophagy, a selective form of autophagy, plays a crucial role in maintaining optimal mitochondrial populations, normal function, and intracellular homeostasis by monitoring and removing damaged or excess mitochondria. Furthermore, mitophagy promotes mitochondrial degradation via the lysosomal pathway, and not only eliminates damaged mitochondria but also regulates programmed cell death-associated genes, thus preventing cell death. The interaction between mitophagy and various forms of cell death has recently gained increasing attention in relation to the pathogenesis of clinical diseases, such as cancers and osteoarthritis, neurodegenerative, cardiovascular, and renal diseases. However, despite the abundant literature on this subject, there is a lack of understanding regarding the interaction between mitophagy and cell death. In this review, we discuss the main pathways of mitophagy, those related to cell death mechanisms (including apoptosis, ferroptosis, and pyroptosis), and the relationship between mitophagy and cell death uncovered in recent years. Our study offers potential directions for therapeutic intervention and disease diagnosis, and contributes to understanding the molecular mechanism of mitophagy. Full article
(This article belongs to the Special Issue New Insights into Reactive Oxygen Species in Cell Death and Immunity)
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28 pages, 6893 KiB  
Review
Mechanism of Reactive Oxygen Species-Guided Immune Responses in Gouty Arthritis and Potential Therapeutic Targets
by Sai Zhang, Daocheng Li, Mingyuan Fan, Jiushu Yuan, Chunguang Xie, Haipo Yuan, Hongyan Xie and Hong Gao
Biomolecules 2024, 14(8), 978; https://doi.org/10.3390/biom14080978 - 9 Aug 2024
Cited by 5 | Viewed by 2773
Abstract
Gouty arthritis (GA) is an inflammatory disease caused by monosodium urate (MSU) crystals deposited in the joint tissues causing severe pain. The disease can recur frequently and tends to form tophus in the joints. Current therapeutic drugs for the acute phase of GA [...] Read more.
Gouty arthritis (GA) is an inflammatory disease caused by monosodium urate (MSU) crystals deposited in the joint tissues causing severe pain. The disease can recur frequently and tends to form tophus in the joints. Current therapeutic drugs for the acute phase of GA have many side effects and limitations, are unable to prevent recurrent GA attacks and tophus formation, and overall efficacy is unsatisfactory. Therefore, we need to advance research on the microscopic mechanism of GA and seek safer and more effective drugs through relevant targets to block the GA disease process. Current research shows that the pathogenesis of GA is closely related to NLRP3 inflammation, oxidative stress, MAPK, NET, autophagy, and Ferroptosis. However, after synthesizing and sorting out the above mechanisms, it is found that the presence of ROS is throughout almost the entire spectrum of micro-mechanisms of the gout disease process, which combines multiple immune responses to form a large network diagram of complex and tight connections involved in the GA disease process. Current studies have shown that inflammation, oxidative stress, cell necrosis, and pathological signs of GA in GA joint tissues can be effectively suppressed by modulating ROS network-related targets. In this article, on the one hand, we investigated the generative mechanism of ROS network generation and its association with GA. On the other hand, we explored the potential of related targets for the treatment of gout and the prevention of tophus formation, which can provide effective reference ideas for the development of highly effective drugs for the treatment of GA. Full article
(This article belongs to the Special Issue New Insights into Reactive Oxygen Species in Cell Death and Immunity)
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