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Nuclear factor (erythroid-derived 2)-like 2 (Nrf2) and exercise
Mallard, Alistair R. ; Spathis, Jemima ; Coombes, Jeff S
Mallard, Alistair R.
Spathis, Jemima
Coombes, Jeff S
Abstract
Chronic metabolic health diseases are increasing worldwide placing strain on healthcare systems and importantly, impacting individuals’ quality of life. It is well established that many chronic diseases are associated with inflammation and oxidative stress. Exercise is a known strategy to manage and treat inflammation in animals and humans. Understanding the mechanisms which cause acute and chronic changes to systems via various exercise protocols may provide insights into how we can better clinically manage patients with inflammatory and oxidative stress associated diseases. Nrf2 is a basic leucine transcription factor which regulates the expression of antioxidant proteins to protect against damage caused by electrophilic or oxidative stress. The aim of this narrative review is to provide an overview of the literature which has investigated the relationship between acute and chronic exercise training and Nrf2 protein, mRNA and Nrf2-ARE binding activity. This narrative review presents analysis of twenty-nine articles presenting studies using animals and humans. Findings from animal models suggest that exercise increases all molecular aspects of the Nrf2-ARE pathway in all tissues studied. It was noted that there seems to be an age-related decline in Nrf2 protein upregulation with exercise training. In humans, however, there is a lack of evidence to support this claim.
Keywords
exercise, resistance exercise, redox control, antioxidant, review, Nrf2, nuclear factor (erythroid-derived 2)-like 2, (Nrf2)
Date
2020
Type
Journal article
Journal
Free Radical Biology & Medicine
Book
Volume
160
Issue
Page Range
471-479
Article Number
ACU Department
School of Behavioural and Health Sciences
Faculty of Health Sciences
Faculty of Health Sciences
Relation URI
Source URL
Event URL
Open Access Status
License
All rights reserved
File Access
Controlled
