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Redox Regulation and Proteostasis in Ageing and Associated Diseases

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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 (31 December 2022) | Viewed by 9008

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Special Issue Editors

Prof. Dr. Haiteng Deng

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Guest Editor

School of Life Sciences, Tsinghua University, Beijing 100084, China
Interests: Development of new techniques in proteomics, metabolomics, and chemical biology; Investigation of redox regulation in aging and associated diseases; Development of novel therapeutic and diagnostic approaches for aging associated diseases
Special Issues, Collections and Topics in MDPI journals

Prof. Dr. Canhua Huang

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Co-Guest Editor

1. School of Basic Medical Sciences, Chengdu University of Traditional Chinese Medicine, Chengdu 611137, China
2. West China School of Basic Medical Sciences and Forensic Medicine, State Key Laboratory of Biotherapy and Cancer Center, West China Hospital and Sichuan University and Collaborative Innovation Center for Biotherapy, Chengdu 610041, China
Interests: redox regulation in tumorigenesis; the mechanism of virus-induced tumorigenesis
Special Issues, Collections and Topics in MDPI journals

Prof. Dr. Bing Zhou

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Co-Guest Editor

Shenzhen Institute of Synthetic Biology, Shenzhen Institute of Advanced Technology, Chinese Academy of Sciences, Shenzhen 518055, China
Interests: homeosastsis of iron and zinc; artemisinins

Special Issue Information

Dear Colleagues,

Loss of redox and protein homeostasis (proteostasis) is a common feature of aging and associated diseases that is characterized by accumulation of cellular damage, unresolved oxidative stress, chronic inflammation and cellular senescence in various tissues. Little is known about how redox homeostasis and proteostasis are challenged during aging and how they are restored with interventions such as exercise, calorie restriction and nutraceuticals. NRF2 has been known as the master regulator of cellular redox homeostasis, but how NRF2 contributes to the onset and progression of age-associated pathologies remains elusive. As the expanded lifespan of the aging population continually imposes challenges on the rapid increase of chronic disease, more research is required to further understand redox regulation and proteostasis in the aged population, to identify specific therapeutic targets for aging, and to uncover plant constituents or other antioxidant molecules and their mechanisms of action for developing new anti-aging strategies.

We cordially invite investigators in the field to contribute original research articles or reviews to this Special Issue of Antioxidants, aiming to understand the landscape of redox homeostasis and proteostasis in aging and associated diseases, to characterize aging-associated redox signaling and protein post-translation modifications, or to identify therapeutic targets or nutraceuticals for aging intervention.

Dr. Haiteng Deng
Prof. Dr. Canhua Huang
Prof. Dr. Bing Zhou
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. Antioxidants 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 2900 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

ageing
cellular senescence
redox regulation
proteostasis
inflammation

Published Papers (4 papers)

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Research

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20 pages, 8841 KiB

Open AccessArticle

Ginsenoside Rg1 Delays Chronological Aging in a Yeast Model via CDC19- and SDH2-Mediated Cellular Metabolism

by Siming Wang, Juhui Qiao, Chunyan Jiang, Daian Pan, Shiting Yu, Jingjing Chen, Shichao Liu, Peiguang Zhang, Daqing Zhao and Meichen Liu

Antioxidants 2023, 12(2), 296; https://doi.org/10.3390/antiox12020296 - 28 Jan 2023

Cited by 3 | Viewed by 1682

Abstract

Ginsenosides, active substances in Panax ginseng C. A. Meyer (ginseng), extend lifespan in multiple species, ameliorate age-associated damage, and limit functional decline in multiple tissues. However, their active components and their molecular mechanisms are largely unknown. Here, ginsenoside Rg1 (Rg1) promoted longevity in Saccharomyces cerevisiae. Treatment with Rg1 decreased aging-mediated surface wrinkling, enhanced stress resistance, decreased reactive oxygen species’ production and apoptosis, improved antioxidant enzyme activity, and decreased the aging rate. Proteomic analysis indicated that Rg1 delays S. cerevisiae senescence by regulating metabolic homeostasis. Protein–protein interaction networks based on differential protein expression indicated that CDC19, a homologue of pyruvate kinase, and SDH2, the succinate dehydrogenase iron–sulfur protein subunit, might be the effector proteins involved in the regulation by Rg1. Further experiments confirmed that Rg1 improved specific parameters of mitochondrial bioenergetics and core enzymes in the glycolytic pathway. Mutant strains were constructed that demonstrated the relationships between metabolic homeostasis and the predicted target proteins of Rg1. Rg1 could be used in new treatments for slowing the aging process. Our results also provide a useful dataset for further investigations of the mechanisms of ginseng in aging. Full article

(This article belongs to the Special Issue Redox Regulation and Proteostasis in Ageing and Associated Diseases)

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14 pages, 3350 KiB

Open AccessArticle

Zinc Protoporphyrin-9 Potentiates the Anticancer Activity of Dihydroartemisinin

by Yu Zhang, Xu Zhang and Bing Zhou

Antioxidants 2023, 12(2), 250; https://doi.org/10.3390/antiox12020250 - 22 Jan 2023

Cited by 1 | Viewed by 1660

Abstract

Besides the clinically proven superior antimalarial activity, artemisinins (ARTs) are also associated with anticancer properties, albeit at much lower potency. Iron and heme have been proposed as possible activators of ARTs against cancer cells. Here we show that zinc protoporphyrin-9 (ZnPPIX), a heme homolog and a natural metabolite for heme synthesis during iron insufficiency, greatly enhanced the anticancer activity of dihydroartemisinin (DHA) in multiple cell lines. Using melanoma B16 and breast cancer 4T1 cells, we demonstrated ZnPPIX dramatically elevated intracellular free heme levels, accompanied by heightened reactive oxidative species (ROS) production. The tumor-suppression activity of ZnPPIX and DHA is mitigated by antioxidant vitamin E or membrane oxidation protectant ferrostatin. In vivo xenograft animal models confirmed that ZnPPIX significantly potentiated the tumor-inhibition capability of DHA while posing no apparent toxicity to the mice. The proliferating index and growth of tumors after the combinatory treatment of DHA and ZnPPIX were evidently reduced. Considering the clinical safety profiles of both DHA and ZnPPIX, their action synergy offers a promising strategy to improve the application of ARTs in our fight against cancer. Full article

(This article belongs to the Special Issue Redox Regulation and Proteostasis in Ageing and Associated Diseases)

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Figure 1

26 pages, 14236 KiB

Open AccessArticle

Aging-Associated Thyroid Dysfunction Contributes to Oxidative Stress and Worsened Functional Outcomes Following Traumatic Brain Injury

by Cheng-Ta Hsieh, Ting-Lin Yen, Yu-Hao Chen, Jing-Shiun Jan, Ruei-Dun Teng, Chih-Hao Yang and Jui-Ming Sun

Antioxidants 2023, 12(2), 217; https://doi.org/10.3390/antiox12020217 - 17 Jan 2023

Cited by 1 | Viewed by 1712

Abstract

The incidence of traumatic brain injury (TBI) increases dramatically with advanced age and accumulating evidence indicates that age is one of the important predictors of an unfavorable prognosis after brain trauma. Unfortunately, thus far, evidence-based effective therapeutics for geriatric TBI is limited. By using middle-aged animals, we first confirm that there is an age-related change in TBI susceptibility manifested by increased inflammatory events, neuronal death and impaired functional outcomes in motor and cognitive behaviors. Since thyroid hormones function as endogenous regulators of oxidative stress, we postulate that age-related thyroid dysfunction could be a crucial pathology in the increased TBI severity. By surgically removing the thyroid glands, which recapitulates the age-related increase in TBI-susceptible phenotypes, we provide direct evidence showing that endogenous thyroid hormone-dependent compensatory regulation of antioxidant events modulates individual TBI susceptibility, which is abolished in aged or thyroidectomized individuals. The antioxidant capacity of melatonin is well-known, and we found acute melatonin treatment but not liothyronine (T3) supplementation improved the TBI-susceptible phenotypes of oxidative stress, excitotoxic neuronal loss and promotes functional recovery in the aged individuals with thyroid dysfunction. Our study suggests that monitoring thyroid function and acute administration of melatonin could be feasible therapeutics in the management of geriatric-TBI in clinic. Full article

(This article belongs to the Special Issue Redox Regulation and Proteostasis in Ageing and Associated Diseases)

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Review

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23 pages, 3259 KiB

Open AccessReview

New Insights into the Gut Microbiota in Neurodegenerative Diseases from the Perspective of Redox Homeostasis

by Yu Wang, Zhe Zhang, Bowen Li, Bo He, Lei Li, Edouard C. Nice, Wei Zhang and Jia Xu

Antioxidants 2022, 11(11), 2287; https://doi.org/10.3390/antiox11112287 - 18 Nov 2022

Cited by 11 | Viewed by 3538

Abstract

An imbalance between oxidants and antioxidants in the body can lead to oxidative stress, which is one of the major causes of neurodegenerative diseases. The gut microbiota contains trillions of beneficial bacteria that play an important role in maintaining redox homeostasis. In the last decade, the microbiota–gut–brain axis has emerged as a new field that has revolutionized the study of the pathology, diagnosis, and treatment of neurodegenerative diseases. Indeed, a growing number of studies have found that communication between the brain and the gut microbiota can be accomplished through the endocrine, immune, and nervous systems. Importantly, dysregulation of the gut microbiota has been strongly associated with the development of oxidative stress-mediated neurodegenerative diseases. Therefore, a deeper understanding of the relationship between the gut microbiota and redox homeostasis will help explain the pathogenesis of neurodegenerative diseases from a new perspective and provide a theoretical basis for proposing new therapeutic strategies for neurodegenerative diseases. In this review, we will describe the role of oxidative stress and the gut microbiota in neurodegenerative diseases and the underlying mechanisms by which the gut microbiota affects redox homeostasis in the brain, leading to neurodegenerative diseases. In addition, we will discuss the potential applications of maintaining redox homeostasis by modulating the gut microbiota to treat neurodegenerative diseases, which could open the door for new therapeutic approaches to combat neurodegenerative diseases. Full article

(This article belongs to the Special Issue Redox Regulation and Proteostasis in Ageing and Associated Diseases)

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