Redox Signaling at the Crossroads of Immunity, Inflammation, Infectious Disease, and Cancer

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 April 2023) | Viewed by 11081

Special Issue Editors

Associate Professor of Microbiology, Lincoln Memorial University—Debusk College of Osteopathic Medicine, 9737 Cogdill Road, Knoxville, TN 37932, USA
Interests: microbiology; oncology; therapeutics
Special Issues, Collections and Topics in MDPI journals
Associate Professor of Pharmacology, Lincoln Memorial University—Debusk College of Osteopathic Medicine, 9737 Cogdill Road, Knoxville, TN 37932, USA
Interests: pharmacology; cardiovascular disease; therapy

Special Issue Information

Dear Colleague,

Reactive oxygen species (ROS) manifest effects that encompass both beneficial physiological functions as well as damaging alterations of cellular components. These two opposing effects of ROS seem to depend on the amount, location, duration, and types of ROS that are generated within the cell. Indeed, normal functioning of the immune system, both innate and adaptive mechanisms, involve acute ROS production and intricately regulated redox signaling. A dysfunctional immune system resulting from oxidative stress and chronic inflammation are now known to be responsible for the initiation, progression, and therapeutic resistance of numerous diseases. However, despite decades of research in this field, no effective therapy is currently approved for regulating altered redox signaling at the crossroads of immunity, inflammation, infectious diseases, and cancer. This Special Issue of Antioxidants will focus on the mechanisms linked to the regulation of pro- and antioxidants in both normal and pathological circumstances. In addition, this Special Issue will address druggable targets that show promise in clinical settings. Therefore, basic research, clinical case reports, as well as review articles will be accepted.

Dr. Debasis Mondal
Dr. Syed Siraj A. Quadri
Guest Editors

Manuscript Submission Information

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Keywords

  • Chronic diseases
  • Inflammation
  • Redox signaling
  • Oxidative stress
  • Autophagy
  • Therapy
  • Side effects
  • Phytochemicals
  • Pharmaceuticals
  • Microbiome
  • Exosome

Published Papers (3 papers)

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Research

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19 pages, 3321 KiB  
Article
Pre-Exposure to Stress-Inducing Agents Increase the Anticancer Efficacy of Focused Ultrasound against Aggressive Prostate Cancer Cells
by Hakm Y. Murad, Partha K. Chandra, Charles A. Kelly, Namrata Khurana, Heng Yu, Emma P. Bortz, Shirley N. Hong, Debasis Mondal and Damir B. Khismatullin
Antioxidants 2022, 11(2), 341; https://doi.org/10.3390/antiox11020341 - 09 Feb 2022
Cited by 3 | Viewed by 1944
Abstract
Despite the initial success in treatment of localized prostate cancer (PCa) using surgery, radiation or hormonal therapy, recurrence of aggressive tumors dictates morbidity and mortality. Focused ultrasound (FUS) is being tested as a targeted, noninvasive approach to eliminate the localized PCa foci, and [...] Read more.
Despite the initial success in treatment of localized prostate cancer (PCa) using surgery, radiation or hormonal therapy, recurrence of aggressive tumors dictates morbidity and mortality. Focused ultrasound (FUS) is being tested as a targeted, noninvasive approach to eliminate the localized PCa foci, and strategies to enhance the anticancer potential of FUS have a high translational value. Since aggressive cancer cells utilize oxidative stress (Ox-stress) and endoplasmic reticulum stress (ER-stress) pathways for their survival and recurrence, we hypothesized that pre-treatment with drugs that disrupt stress-signaling pathways in tumor cells may increase FUS efficacy. Using four different PCa cell lines, i.e., LNCaP, C4-2B, 22Rv1 and DU145, we tested the in vitro effects of FUS, alone and in combination with two clinically tested drugs that increase Ox-stress (i.e., CDDO-me) or ER-stress (i.e., nelfinavir). As compared to standalone FUS, significant (p < 0.05) suppressions in both survival and recurrence of PCa cells were observed following pre-sensitization with low-dose CDDO-me (100 nM) and/or nelfinavir (2 µM). In drug pre-sensitized cells, significant anticancer effects were evident at a FUS intensity of as low as 0.7 kW/cm2. This combined mechanochemical disruption (MCD) approach decreased cell proliferation, migration and clonogenic ability and increased apoptosis/necrosis and reactive oxygen species (ROS) production. Furthermore, although activated in cells that survived standalone FUS, pre-sensitization with CDDO-me and/or nelfinavir suppressed both total and activated (phosphorylated) NF-κB and Akt protein levels. Thus, a combined MCD therapy may be a safe and effective approach towards the targeted elimination of aggressive PCa cells. Full article
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Review

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27 pages, 3666 KiB  
Review
Tetrahydrobiopterin: Beyond Its Traditional Role as a Cofactor
by Tuany Eichwald, Lucila de Bortoli da Silva, Ananda Christina Staats Pires, Laís Niero, Erick Schnorrenberger, Clovis Colpani Filho, Gisele Espíndola, Wei-Lin Huang, Gilles J. Guillemin, José E. Abdenur and Alexandra Latini
Antioxidants 2023, 12(5), 1037; https://doi.org/10.3390/antiox12051037 - 03 May 2023
Cited by 12 | Viewed by 4460
Abstract
Tetrahydrobiopterin (BH4) is an endogenous cofactor for some enzymatic conversions of essential biomolecules, including nitric oxide, and monoamine neurotransmitters, and for the metabolism of phenylalanine and lipid esters. Over the last decade, BH4 metabolism has emerged as a promising metabolic target for negatively [...] Read more.
Tetrahydrobiopterin (BH4) is an endogenous cofactor for some enzymatic conversions of essential biomolecules, including nitric oxide, and monoamine neurotransmitters, and for the metabolism of phenylalanine and lipid esters. Over the last decade, BH4 metabolism has emerged as a promising metabolic target for negatively modulating toxic pathways that may result in cell death. Strong preclinical evidence has shown that BH4 metabolism has multiple biological roles beyond its traditional cofactor activity. We have shown that BH4 supports essential pathways, e.g., to generate energy, to enhance the antioxidant resistance of cells against stressful conditions, and to protect from sustained inflammation, among others. Therefore, BH4 should not be understood solely as an enzyme cofactor, but should instead be depicted as a cytoprotective pathway that is finely regulated by the interaction of three different metabolic pathways, thus assuring specific intracellular concentrations. Here, we bring state-of-the-art information about the dependency of mitochondrial activity upon the availability of BH4, as well as the cytoprotective pathways that are enhanced after BH4 exposure. We also bring evidence about the potential use of BH4 as a new pharmacological option for diseases in which mitochondrial disfunction has been implicated, including chronic metabolic disorders, neurodegenerative diseases, and primary mitochondriopathies. Full article
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14 pages, 696 KiB  
Review
Statins’ Regulation of the Virulence Factors of Helicobacter pylori and the Production of ROS May Inhibit the Development of Gastric Cancer
by Ting-Yu Lin, Wen-Hsi Lan, Ya-Fang Chiu, Chun-Lung Feng, Cheng-Hsun Chiu, Chia-Jung Kuo and Chih-Ho Lai
Antioxidants 2021, 10(8), 1293; https://doi.org/10.3390/antiox10081293 - 16 Aug 2021
Cited by 8 | Viewed by 3219
Abstract
Conventionally, statins are used to treat high cholesterol levels. They exhibit pleiotropic effects, such as the prevention of cardiovascular disease and decreased cancer mortality. Gastric cancer (GC) is one of the most common cancers, ranking as the third leading global cause of cancer-related [...] Read more.
Conventionally, statins are used to treat high cholesterol levels. They exhibit pleiotropic effects, such as the prevention of cardiovascular disease and decreased cancer mortality. Gastric cancer (GC) is one of the most common cancers, ranking as the third leading global cause of cancer-related deaths, and is mainly attributed to chronic Helicobacter pylori infection. During their co-evolution with hosts, H. pylori has developed the ability to use the cellular components of the host to evade the immune system and multiply in intracellular niches. Certain H. pylori virulence factors, including cytotoxin-associated gene A (CagA), vacuolating cytotoxin A (VacA), and cholesterol-α-glucosyltransferase (CGT), have been shown to exploit host cholesterol during pathogenesis. Therefore, using statins to antagonize cholesterol synthesis might prove to be an ideal strategy for reducing the occurrence of H. pylori-related GC. This review discusses the current understanding of the interplay of H. pylori virulence factors with cholesterol and reactive oxygen species (ROS) production, which may prove to be novel therapeutic targets for the development of effective treatment strategies against H. pylori-associated GC. We also summarize the findings of several clinical studies on the association between statin therapy and the development of GC, especially in terms of cancer risk and mortality. Full article
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