Oxidative Stress and Aging

A special issue of Antioxidants (ISSN 2076-3921).

Deadline for manuscript submissions: closed (31 July 2018) | Viewed by 8772

Special Issue Editor


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Guest Editor
Brain Ageing Research Laboratory, Centre for Healthy Brain Ageing, School of Psychiatry, Faculty of Medicine, University of New South Wales, Sydney 2052, Australia
Interests: oxidative stress; aging; neurosciences; neurodegeneration; inflammation; antioxidants; polyphenols; Alzheimer's disease; gene expression; multi-omics; biomarkers
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Special Issue Information

Dear Colleagues,

Numerous studies have shown that oxidative stress is a key factor in cellular degeneration. The accumulation of chronic oxidative stress leads to deleterious cellular processes associated with ageing and a wide variety of age-related degenerative diseases. Oxidative damage to our cells as a result of poor diet and lifestyle choices are likely to accelerate ageing and lead to the development of degenerative diseases.

There has been a growing awareness of the role of naturally occurring compounds as attractive targets that may prevent or slow down cellular loss. Further investigation in this subject will provide renewed insight on the implication of oxidative stress in degenerative disorders, and contribute to the growing awareness of the role of natural botanicals as future therapies for neurodegeneration and brain ageing.

We invite authors to submit original research and review articles that seek to improve our understanding of the role of oxidative stress, excitotoxicity, mitochondrial function, antioxidants, polyphenols and inflammation in the pathophysiology of age-related disorders.

Potential topics include, but are not limited to:

  • Research in mitochondrial function and cellular respiration, reactive oxygen species, and nitric oxide on cell viability;
  • Recent advances on the impact of oxidative stress in degenerative disorders;
  • Role of inflammatory mediators in free radical generation;
  • Recent developments in natural occurring phytochemicals as degenerative diseases therapies.
Dr. Nady Braidy
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.

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
  • Antioxidants
  • Oxidative Stress
  • Inflammation
  • Polyphenols
  • Sirtuins
  • NAD+

Published Papers (1 paper)

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Review

16 pages, 1277 KiB  
Review
Redox Signaling of NADPH Oxidases Regulates Oxidative Stress Responses, Immunity and Aging
by Collin Y. Ewald
Antioxidants 2018, 7(10), 130; https://doi.org/10.3390/antiox7100130 - 28 Sep 2018
Cited by 48 | Viewed by 8262
Abstract
An accumulating body of evidence suggests that transient or physiological reactive oxygen species (ROS) generated by nicotinamide adenine dinucleotide phosphate (NADPH) oxidases act as a redox signal to re-establish homeostasis. The capacity to re-establish homeostasis progressively declines during aging but is maintained in [...] Read more.
An accumulating body of evidence suggests that transient or physiological reactive oxygen species (ROS) generated by nicotinamide adenine dinucleotide phosphate (NADPH) oxidases act as a redox signal to re-establish homeostasis. The capacity to re-establish homeostasis progressively declines during aging but is maintained in long-lived animals to promote healthy aging. In the model organism Caenorhabditis elegans, ROS generated by dual oxidases (Duox) are important for extracellular matrix integrity, pathogen defense, oxidative stress resistance, and longevity. The Duox enzymatic activity is tightly regulated and under cellular control. Developmental molting cycles, pathogen infections, toxins, mitochondrial-derived ROS, drugs, and small GTPases (e.g., RHO-1) can activate Duox (BLI-3) to generate ROS, whereas NADPH oxidase inhibitors and negative regulators, such as MEMO-1, can inhibit Duox from generating ROS. Three mechanisms-of-action have been discovered for the Duox/BLI-3-generated ROS: (1) enzymatic activity to catalyze crosslinking of free tyrosine ethyl ester in collagen bundles to stabilize extracellular matrices, (2) high ROS bursts/levels to kill pathogens, and (3) redox signaling activating downstream kinase cascades to transcription factors orchestrating oxidative stress and immunity responses to re-establish homeostasis. Although Duox function at the cell surface is well established, recent genetic and biochemical data also suggests a novel role for Duoxs at the endoplasmic reticulum membrane to control redox signaling. Evidence underlying these mechanisms initiated by ROS from NADPH oxidases, and their relevance for human aging, are discussed in this review. Appropriately controlling NADPH oxidase activity for local and physiological redox signaling to maintain cellular homeostasis might be a therapeutic strategy to promote healthy aging. Full article
(This article belongs to the Special Issue Oxidative Stress and Aging)
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