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Reactive Oxygen Species and Oxidative Stress in Cellular Homeostasis and...
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Reactive Oxygen Species and Oxidative Stress in Cellular Homeostasis and Pathophysiology

A special issue of Cells (ISSN 2073-4409). This special issue belongs to the section "Cellular Pathology".

Deadline for manuscript submissions: closed (30 November 2023) | Viewed by 8835

Special Issue Editor

Dr. Nikolaos Georgopoulos

E-Mail Website
Guest Editor
Department of Biological Sciences, School of Applied Sciences, University of Huddersfield, Huddersfield, UK
Interests: cell biology; cancer research; immunology; epithelial tissues; cell death tissue engineering; skin

Special Issue Information

Dear Colleagues,

Reactive oxygen species (ROS) represent the main group of cellular oxidants, and are free radicals generated within cells. ROS are key components of cellular (redox) signaling and play important roles in cellular homeostasis. They are involved in cell survival (including processes such as wound healing) and cell death (e.g., apoptosis, ferroptosis), as well as immunological responses (e.g., cell proliferation, pathogen elimination), in addition to having key roles in vascular homeostasis (by regulation of endothelial and smooth-muscle-cell functions). To counteract the action of ROS and avoid oxidative injury, cells utilize antioxidant mechanisms which have evolved as defenses that detoxify oxidants to prevent or repair oxidative damage. Oxidative stress represents a shift in the dynamic balance between the production of oxidants and antioxidant defenses. The main consequence of this imbalance is oxidative damage, which is linked to cellular toxicity as well as a number of pathological conditions.

In this Special Issue, we overview the multiplicity of roles for ROS in human health and disease by highlighting the molecular functions of ROS in normal redox signaling as well as discussing how the deregulation of redox signaling can underpin pathophysiology.   

Dr. Nikolaos Georgopoulos
Guest Editor

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. Cells is an international peer-reviewed open access semimonthly 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
  • oxidative stress
  • redox signaling
  • proliferation
  • cell death
  • homeostasis
  • disease pathology

Published Papers (4 papers)

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Research

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17 pages, 6144 KiB  
Article
Attenuation of Oxidative Damage via Upregulating Nrf2/HO-1 Signaling Pathway by Protease SH21 with Exerting Anti-Inflammatory and Anticancer Properties In Vitro
by Hasan Tarek, Seung Sik Cho, Md. Selim Hossain and Jin Cheol Yoo
Cells 2023, 12(17), 2190; https://doi.org/10.3390/cells12172190 - 1 Sep 2023
Cited by 4 | Viewed by 1218
Abstract
Oxidative damage and inflammation are among the very significant aspects interrelated with cancer and other degenerative diseases. In this study, we investigated the biological activities of a 25 kDa protease (SH21) that was purified from Bacillus siamensis. SH21 exhibited very powerful antioxidant [...] Read more.
Oxidative damage and inflammation are among the very significant aspects interrelated with cancer and other degenerative diseases. In this study, we investigated the biological activities of a 25 kDa protease (SH21) that was purified from Bacillus siamensis. SH21 exhibited very powerful antioxidant and reactive oxygen species (ROS) generation inhibition activity in a dose-dependent approach. The mRNA and protein levels of antioxidant enzymes such as superoxide dismutase 1 (SOD1), catalase (CAT), and glutathione peroxidase 1 (GPx-1) were enhanced in the SH21-treated sample. SH21 also increased the transcriptional and translational activities of NF-E2-related factor 2 (Nrf2) with the subsequent development of detoxifying enzyme heme oxygenase-1 (HO-1). In addition, SH21 showed potential anti-inflammatory activity via inhibition of nitric oxide (NO) and proinflammatory cytokines, such as TNF-α, IL-6, and IL-1β, production in lipopolysaccharide (LPS)-stimulated RAW 264.7 cells. At concentrations of 60, 80, and 100 μg/mL, SH21 potentially suppressed nitric oxide synthase (iNOS) and cytokine gene expressions. Furthermore, SH21 significantly released lactate dehydrogenase (LDH) enzyme in cancer cell supernatant in a concentration-dependent manner and showed strong activity against three tested cancer cell lines, including HL-60, A549, and Hela. Our results suggest that SH21 has effective antioxidant, anti-inflammatory, and anticancer effects and could be an excellent therapeutic agent against inflammation-related diseases. Full article
(This article belongs to the Special Issue Reactive Oxygen Species and Oxidative Stress in Cellular Homeostasis and Pathophysiology)
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16 pages, 4494 KiB  
Article
Phytol Suppresses Osteoclast Differentiation and Oxidative Stress through Nrf2/HO-1 Regulation in RANKL-Induced RAW264.7 Cells
by Eun-Nam Kim, Nguyen Minh Trang, Heesun Kang, Ki Hyun Kim and Gil-Saeng Jeong
Cells 2022, 11(22), 3596; https://doi.org/10.3390/cells11223596 - 14 Nov 2022
Cited by 10 | Viewed by 2387
Abstract
Osteoporosis is a systemic skeletal disorder where osteoclasts are prevalent among osteoblasts. Oxidative stress is one of the main causes of osteoporosis, and nuclear factor erythroid-2-related factor 2 (Nrf2) is the master regulator of antioxidant responses. Phytol, a diterpene isolated from Stevia rebaudiana [...] Read more.
Osteoporosis is a systemic skeletal disorder where osteoclasts are prevalent among osteoblasts. Oxidative stress is one of the main causes of osteoporosis, and nuclear factor erythroid-2-related factor 2 (Nrf2) is the master regulator of antioxidant responses. Phytol, a diterpene isolated from Stevia rebaudiana leaves, has many biological effects, including antimicrobial, antioxidant, and anti-inflammatory effects. This study investigated the crosstalk between Nrf2 and osteoclast differentiation in the presence of phytol. Phytol inhibited osteoclast differentiation through TRAP-positive and F-actin formation. The expression of anti-nuclear factor of activated T cells-c1 (NFATc1) and c-Fos was suppressed by phytol, as shown using Western blot and RT-PCR analysis. Phytol inhibited oxidative stress by suppressing reactive oxidant species (ROS) accumulation while recovering antioxidant enzymes, including superoxide dismutase and catalase. Additionally, phytol ameliorated osteoclast-specific differentiation, function, and oxidative stress through Nrf2 regulation by siRNA transfection. In conclusion, these data demonstrate the inhibitory effect of phytol on osteoclast differentiation through Nrf2 regulation, suggesting its potential use in oxidative stress-related osteoporosis and bone diseases. Full article
(This article belongs to the Special Issue Reactive Oxygen Species and Oxidative Stress in Cellular Homeostasis and Pathophysiology)
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19 pages, 3414 KiB  
Article
TRAF3/p38-JNK Signalling Crosstalk with Intracellular-TRAIL/Caspase-10-Induced Apoptosis Accelerates ROS-Driven Cancer Cell-Specific Death by CD40
by Khalidah Ibraheem, Albashir M. A. Yhmed, Mohamed M. Nasef and Nikolaos T. Georgopoulos
Cells 2022, 11(20), 3274; https://doi.org/10.3390/cells11203274 - 18 Oct 2022
Cited by 9 | Viewed by 2129
Abstract
The capacity to induce tumour-cell specific apoptosis represents the most unique feature of the TNF receptor (TNFR) family member CD40. Recent studies on the signalling events triggered by its membrane-presented ligand CD40L (mCD40L) in normal and malignant epithelial cells have started to unravel [...] Read more.
The capacity to induce tumour-cell specific apoptosis represents the most unique feature of the TNF receptor (TNFR) family member CD40. Recent studies on the signalling events triggered by its membrane-presented ligand CD40L (mCD40L) in normal and malignant epithelial cells have started to unravel an exquisite context and cell type specificity for the functional effects of CD40. Here, we demonstrate that, in comparison to other carcinomas, mCD40L triggered strikingly more rapid apoptosis in colorectal carcinoma (CRC) cells, underpinned by its ability to entrain two concurrently operating signalling axes. CD40 ligation initially activates TNFR-associated factor 3 (TRAF3) and subsequently NADPH oxidase (NOX)/Apoptosis signal-regulating kinase 1 (ASK1)-signalling and induction of reactive oxygen species (ROS) to mediate p38/JNK- and ROS-dependent cell death. At that point, p38/JNK signalling directly activates the mitochondrial pathway, and triggers rapid induction of intracellular TNF-related apoptosis-inducing ligand (TRAIL) that signals from internal compartments to initiate extrinsic caspase-10-asscociated apoptosis, leading to truncated Bid (tBid)-activated mitochondrial signalling. p38 and JNK are essential both for direct mitochondrial apoptosis induction and the TRAIL/caspase-10/tBid pathway, but their involvement follows functional hierarchy and temporally controlled interplay, as p38 function is required for JNK phosphorylation. By engaging both intrinsic and extrinsic pathways to activate apoptosis via two signals simultaneously, CD40 can accelerate CRC cell death. Our findings further unravel the multi-faceted properties of the CD40/mCD40L dyad, highlighted by the novel TNFR crosstalk that accelerates tumour cell-specific death, and may have implications for the use of CD40 as a therapeutic target. Full article
(This article belongs to the Special Issue Reactive Oxygen Species and Oxidative Stress in Cellular Homeostasis and Pathophysiology)
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Review

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22 pages, 1620 KiB  
Review
The Gut–Brain Axis as a Therapeutic Target in Multiple Sclerosis
by Ana Maria Buga, Vlad Padureanu, Anca-Lelia Riza, Carmen Nicoleta Oancea, Carmen Valeria Albu and Alexandru Dan Nica
Cells 2023, 12(14), 1872; https://doi.org/10.3390/cells12141872 - 17 Jul 2023
Cited by 2 | Viewed by 2242
Abstract
The CNS is very susceptible to oxidative stress; the gut microbiota plays an important role as a trigger of oxidative damage that promotes mitochondrial dysfunction, neuroinflammation, and neurodegeneration. In the current review, we discuss recent findings on oxidative-stress-related inflammation mediated by the gut–brain [...] Read more.
The CNS is very susceptible to oxidative stress; the gut microbiota plays an important role as a trigger of oxidative damage that promotes mitochondrial dysfunction, neuroinflammation, and neurodegeneration. In the current review, we discuss recent findings on oxidative-stress-related inflammation mediated by the gut–brain axis in multiple sclerosis (MS). Growing evidence suggests targeting gut microbiota can be a promising strategy for MS management. Intricate interaction between multiple factors leads to increased intra- and inter-individual heterogeneity, frequently painting a different picture in vivo from that obtained under controlled conditions. Following an evidence-based approach, all proposed interventions should be validated in clinical trials with cohorts large enough to reach significance. Our review summarizes existing clinical trials focused on identifying suitable interventions, the suitable combinations, and appropriate timings to target microbiota-related oxidative stress. Most studies assessed relapsing–remitting MS (RRMS); only a few studies with very limited cohorts were carried out in other MS stages (e.g., secondary progressive MS–SPMS). Future trials must consider an extended time frame, perhaps starting with the perinatal period and lasting until the young adult period, aiming to capture as many complex intersystem interactions as possible. Full article
(This article belongs to the Special Issue Reactive Oxygen Species and Oxidative Stress in Cellular Homeostasis and Pathophysiology)
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