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Antioxidants
Special Issues
Oxidative Stress and Cell Senescence Process
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Oxidative Stress and Cell Senescence Process

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 June 2022) | Viewed by 33001

Special Issue Editor

Dr. Raffaella Faraonio

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Guest Editor
Department of Molecular Medicine and Medical Biotechnologies, University of Naples Federico II, 80131 Naples, Italy
Interests: oxidative stress; cellular senescence; transcription factors; non-coding RNAs; chromatin remodeling factors
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues, 

Oxidative stress occurs when the production of reactive oxygen species/reactive nitrogen species (ROS/RNS) overwhelms the endogenous antioxidant defenses. Under physiological conditions, the amounts of ROS/RNS are finely controlled, and redox signaling mediates proper cellular function. “Redox Homeostasis” indicates molecular mechanisms that constantly scavenge ROS/RNS molecules, providing cell equilibrium between their production and clearance/inactivation. Over the last few decades, overwhelming research has evidenced a central role of oxidative stress in a number of physiopathological events, including telomere-independent cell senescence process. Cell senescence represents, at least early in life, a safety program to permanently arrest damaged cells but is a key contributor to aging and age-related diseases.

The senescence process is sustained by a reprogrammed gene expression, involving transcriptional and post-transcriptional mechanisms as well as epigenetic regulatory events. This Special Issue aims to describe new redox-sensitive players (transcription factors, noncoding RNAs, chromatin remodeling factors) and novel molecular pathways in boosting or delaying cell senescence. Even though exactly the opposite, both types of signaling could share essential factors/molecules whose activities could influence or be influenced by ROS/RNS levels.

This will contribute to extend emerging evidence concerning the use of synthetic molecules for in vivo delivery or antioxidant supplementation with future therapeutic purposes. 

Dr. Raffaella Faraonio
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. Antioxidants is an international peer-reviewed open access monthly journal published by MDPI.

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Published Papers (7 papers)

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Editorial

Jump to: Research, Review

3 pages, 206 KiB  
Editorial
Oxidative Stress and Cell Senescence Process
by Raffaella Faraonio
Antioxidants 2022, 11(9), 1718; https://doi.org/10.3390/antiox11091718 - 30 Aug 2022
Cited by 18 | Viewed by 2025
Abstract
Oxidative stress due to excessive amounts of reactive oxygen species (ROS) and reactive nitrogen species (RNS) plays a leading role in damages to macromolecules and, as such, it represents a key driver of numerous physio-pathological events, including cellular senescence [...] Full article
(This article belongs to the Special Issue Oxidative Stress and Cell Senescence Process)

Research

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14 pages, 7676 KiB  
Article
Resolvin D1 Suppresses H2O2-Induced Senescence in Fibroblasts by Inducing Autophagy through the miR-1299/ARG2/ARL1 Axis
by Hyun Ji Kim, Boram Kim, Hyung Jung Byun, Lu Yu, Tuan Minh Nguyen, Thi Ha Nguyen, Phuong Anh Do, Eun Ji Kim, Kyung Ah Cheong, Kyung Sung Kim, Hiệu Huy Phùng, Mostafizur Rahman, Ji Yun Jang, Seung Bae Rho, Gyeoung Jin Kang, Mi Kyung Park, Ho Lee, Kyeong Lee, Jungsook Cho, Hyo Kyung Han, Sang Geon Kim, Ai Young Lee and Chang Hoon Leeadd Show full author list remove Hide full author list
Antioxidants 2021, 10(12), 1924; https://doi.org/10.3390/antiox10121924 - 30 Nov 2021
Cited by 15 | Viewed by 3605
Abstract
ARG2 has been reported to inhibit autophagy in vascular endothelial cells and keratinocytes. However, studies of its mechanism of action, its role in skin fibroblasts, and the possibility of promoting autophagy and inhibiting cellular senescence through ARG2 inhibition are lacking. We induced cellular [...] Read more.
ARG2 has been reported to inhibit autophagy in vascular endothelial cells and keratinocytes. However, studies of its mechanism of action, its role in skin fibroblasts, and the possibility of promoting autophagy and inhibiting cellular senescence through ARG2 inhibition are lacking. We induced cellular senescence in dermal fibroblasts by using H2O2. H2O2-induced fibroblast senescence was inhibited upon ARG2 knockdown and promoted upon ARG2 overexpression. The microRNA miR-1299 suppressed ARG2 expression, thereby inhibiting fibroblast senescence, and miR-1299 inhibitors promoted dermal fibroblast senescence by upregulating ARG2. Using yeast two-hybrid assay, we found that ARG2 binds to ARL1. ARL1 knockdown inhibited autophagy and ARL1 overexpression promoted it. Resolvin D1 (RvD1) suppressed ARG2 expression and cellular senescence. These data indicate that ARG2 stimulates dermal fibroblast cell senescence by inhibiting autophagy after interacting with ARL1. In addition, RvD1 appears to promote autophagy and inhibit dermal fibroblast senescence by inhibiting ARG2 expression. Taken together, the miR-1299/ARG2/ARL1 axis emerges as a novel mechanism of the ARG2-induced inhibition of autophagy. Furthermore, these results indicate that miR-1299 and pro-resolving lipids, including RvD1, are likely involved in inhibiting cellular senescence by inducing autophagy. Full article
(This article belongs to the Special Issue Oxidative Stress and Cell Senescence Process)
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15 pages, 2693 KiB  
Article
Camphorquinone Promotes the Antisenescence Effect via Activating AMPK/SIRT1 in Stem Cells and D-Galactose-Induced Aging Mice
by Nagarajan Maharajan and Gwang-Won Cho
Antioxidants 2021, 10(12), 1916; https://doi.org/10.3390/antiox10121916 - 29 Nov 2021
Cited by 13 | Viewed by 2948
Abstract
Terpenoids are a wide class of secondary metabolites with geroprotective properties that can alter the mechanism of aging and aging-related diseases. Camphorquinone (CQ) is a bicyclic monoterpenoid compound that can be efficiently synthesized through the continuous bromination and oxidation reaction of camphor. The [...] Read more.
Terpenoids are a wide class of secondary metabolites with geroprotective properties that can alter the mechanism of aging and aging-related diseases. Camphorquinone (CQ) is a bicyclic monoterpenoid compound that can be efficiently synthesized through the continuous bromination and oxidation reaction of camphor. The purpose of this study is to investigate the effects of CQ on oxidative-stress-induced senescence and its underlying mechanisms. To generate oxidative stress in human bone marrow mesenchymal stem cells (hBM-MSCs) and mice, we used hydrogen peroxide (200 μM twice) and D-galactose (D-Gal) (150 mg/kg for 10 weeks), respectively. Our findings suggest that CQ potentially reduces senescence in hBM-MSCs and mouse heart tissue. In addition, we found that CQ boosted AMPK/SIRT1 activation and autophagy in both models. These results were subsequently verified in hBM-MSCs using compound C (an AMPK inhibitor) but AMPK inhibition by CC did not significantly reduce the SIRT1 and the autophagy markers. CQ treatment also reduced the gene expression of inflammation markers in D-Gal-induced aging mouse heart tissue. Furthermore, we determined that CQ fits all of the pharmacological parameters using the freely available SwissADME Web tool. Collectively, our findings demonstrate that CQ possesses antisenescence and cardioprotective properties, and that oxidative-stress-induced senescence could be suppressed by AMPK/SIRT1 and autophagy mechanisms. Full article
(This article belongs to the Special Issue Oxidative Stress and Cell Senescence Process)
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13 pages, 2418 KiB  
Article
FK866 Protects Human Dental Pulp Cells against Oxidative Stress-Induced Cellular Senescence
by Chang Youp Ok, Sera Park, Hye-Ock Jang, Takashi Takata, Ok-Hee Lee, Moon-Kyoung Bae and Soo-Kyung Bae
Antioxidants 2021, 10(2), 271; https://doi.org/10.3390/antiox10020271 - 10 Feb 2021
Cited by 13 | Viewed by 3160
Abstract
FK866 possesses various functional properties, such as anti-angiogenic, anti-cancer, and anti-inflammatory activities. We previously demonstrated that premature senescence of human dental pulp cells (hDPCs) was induced by hydrogen peroxide (H2O2). The present study aimed to investigate whether H2 [...] Read more.
FK866 possesses various functional properties, such as anti-angiogenic, anti-cancer, and anti-inflammatory activities. We previously demonstrated that premature senescence of human dental pulp cells (hDPCs) was induced by hydrogen peroxide (H2O2). The present study aimed to investigate whether H2O2-induced premature senescence of hDPCs is affected by treatment with FK866. We found that FK866 markedly inhibited the senescent characteristics of hDPCs after exposure to H2O2, as revealed by an increase in the number of senescence-associated β-galactosidase (SA-β-gal)-positive hDPCs and the upregulation of the p21 and p53 proteins, which acts as molecular indicators of cellular senescence. Moreover, the stimulatory effects of H2O2 on cellular senescence are associated with oxidative stress induction, such as excessive ROS production and NADPH consumption, telomere DNA damage induction, and upregulation of senescence-associated secretory phenotype factors (IL-1β, IL-6, IL-8, COX-2, and TNF-α) as well as NF-κB activation, which were all blocked by FK866. Thus, FK866 might antagonize H2O2-induced premature senescence of hDPCs, acting as a potential therapeutic antioxidant by attenuating oxidative stress-induced pathologies in dental pulp, including inflammation and cellular senescence. Full article
(This article belongs to the Special Issue Oxidative Stress and Cell Senescence Process)
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16 pages, 4049 KiB  
Article
Exogenous NAD+ Postpones the D-Gal-Induced Senescence of Bone Marrow-Derived Mesenchymal Stem Cells via Sirt1 Signaling
by Jie Wang, Lin Liu, Zhongjie Ding, Qing Luo, Yang Ju and Guanbin Song
Antioxidants 2021, 10(2), 254; https://doi.org/10.3390/antiox10020254 - 7 Feb 2021
Cited by 16 | Viewed by 2970
Abstract
Cell senescence is accompanied by decreased nicotinamide adenine dinucleotide (NAD+) levels; however, whether exogenous NAD+ affects bone marrow-derived mesenchymal stem cells (BMSCs) senescence and the involved mechanisms is still unclear. Here, we find that exogenous NAD+ replenishment significantly postpones [...] Read more.
Cell senescence is accompanied by decreased nicotinamide adenine dinucleotide (NAD+) levels; however, whether exogenous NAD+ affects bone marrow-derived mesenchymal stem cells (BMSCs) senescence and the involved mechanisms is still unclear. Here, we find that exogenous NAD+ replenishment significantly postpones BMSC senescence induced by D-galactose (D-gal). It is also shown that exogenous NAD+ leads to increased intracellular NAD+ levels and reduced intracellular reactive oxygen species in senescent BMSCs here. Further investigation showed that exogenous NAD+ weakened BMSC senescence by increasing Sirtuin 1 (Sirt1) expression. Moreover, exogenous NAD+ reduced senescence-associated-β-galactosidase activity, and downregulated poly (ADP-ribose) polymerase 1 expression. In addition, the reduced expression of Sirt1 by small interfering RNA abolished the beneficial effects of exogenous NAD+ in terms of postponing BMSCs senescence induced by D-gal. Taken together, our results indicate that exogenous NAD+ could postpone D-gal-induced BMSC senescence through Sirt1 signaling, providing a potential method for obtaining high quality BMSCs to support their research and clinical application. Full article
(This article belongs to the Special Issue Oxidative Stress and Cell Senescence Process)
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Review

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42 pages, 2494 KiB  
Review
The Role of Antioxidants in the Interplay between Oxidative Stress and Senescence
by Angelica Varesi, Salvatore Chirumbolo, Lucrezia Irene Maria Campagnoli, Elisa Pierella, Gaia Bavestrello Piccini, Adelaide Carrara, Giovanni Ricevuti, Catia Scassellati, Cristian Bonvicini and Alessia Pascale
Antioxidants 2022, 11(7), 1224; https://doi.org/10.3390/antiox11071224 - 22 Jun 2022
Cited by 58 | Viewed by 12971
Abstract
Cellular senescence is an irreversible state of cell cycle arrest occurring in response to stressful stimuli, such as telomere attrition, DNA damage, reactive oxygen species, and oncogenic proteins. Although beneficial and protective in several physiological processes, an excessive senescent cell burden has been [...] Read more.
Cellular senescence is an irreversible state of cell cycle arrest occurring in response to stressful stimuli, such as telomere attrition, DNA damage, reactive oxygen species, and oncogenic proteins. Although beneficial and protective in several physiological processes, an excessive senescent cell burden has been involved in various pathological conditions including aging, tissue dysfunction and chronic diseases. Oxidative stress (OS) can drive senescence due to a loss of balance between pro-oxidant stimuli and antioxidant defences. Therefore, the identification and characterization of antioxidant compounds capable of preventing or counteracting the senescent phenotype is of major interest. However, despite the considerable number of studies, a comprehensive overview of the main antioxidant molecules capable of counteracting OS-induced senescence is still lacking. Here, besides a brief description of the molecular mechanisms implicated in OS-mediated aging, we review and discuss the role of enzymes, mitochondria-targeting compounds, vitamins, carotenoids, organosulfur compounds, nitrogen non-protein molecules, minerals, flavonoids, and non-flavonoids as antioxidant compounds with an anti-aging potential, therefore offering insights into innovative lifespan-extending approaches. Full article
(This article belongs to the Special Issue Oxidative Stress and Cell Senescence Process)
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34 pages, 2071 KiB  
Review
MicroRNAs, Long Non-Coding RNAs, and Circular RNAs in the Redox Control of Cell Senescence
by Daniele Lettieri-Barbato, Katia Aquilano, Carolina Punziano, Giuseppina Minopoli and Raffaella Faraonio
Antioxidants 2022, 11(3), 480; https://doi.org/10.3390/antiox11030480 - 28 Feb 2022
Cited by 23 | Viewed by 3806
Abstract
Cell senescence is critical in diverse aspects of organism life. It is involved in tissue development and homeostasis, as well as in tumor suppression. Consequently, it is tightly integrated with basic physiological processes during life. On the other hand, senescence is gradually being [...] Read more.
Cell senescence is critical in diverse aspects of organism life. It is involved in tissue development and homeostasis, as well as in tumor suppression. Consequently, it is tightly integrated with basic physiological processes during life. On the other hand, senescence is gradually being considered as a major contributor of organismal aging and age-related diseases. Increased oxidative stress is one of the main risk factors for cellular damages, and thus a driver of senescence. In fact, there is an intimate link between cell senescence and response to different types of cellular stress. Oxidative stress occurs when the production of reactive oxygen species/reactive nitrogen species (ROS/RNS) is not adequately detoxified by the antioxidant defense systems. Non-coding RNAs are endogenous transcripts that govern gene regulatory networks, thus impacting both physiological and pathological events. Among these molecules, microRNAs, long non-coding RNAs, and more recently circular RNAs are considered crucial mediators of almost all cellular processes, including those implicated in oxidative stress responses. Here, we will describe recent data on the link between ROS/RNS-induced senescence and the current knowledge on the role of non-coding RNAs in the senescence program. Full article
(This article belongs to the Special Issue Oxidative Stress and Cell Senescence Process)
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