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Dietary Regulation of Keap1/Nrf2/ARE Pathway: Focus on Plant-Derived Compounds and Trace Minerals
It has become increasingly evident that chronic inflammation underpins the development of many chronic diseases including cancer, cardiovascular disease and type 2 diabetes. Oxidative stress is inherently a biochemical dysregulation of the redox status of the intracellular environment, which under h...
Autores principales: | , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
MDPI
2014
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4179188/ https://www.ncbi.nlm.nih.gov/pubmed/25244368 http://dx.doi.org/10.3390/nu6093777 |
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author | Stefanson, Amanda L. Bakovic, Marica |
author_facet | Stefanson, Amanda L. Bakovic, Marica |
author_sort | Stefanson, Amanda L. |
collection | PubMed |
description | It has become increasingly evident that chronic inflammation underpins the development of many chronic diseases including cancer, cardiovascular disease and type 2 diabetes. Oxidative stress is inherently a biochemical dysregulation of the redox status of the intracellular environment, which under homeostatic conditions is a reducing environment, whereas inflammation is the biological response to oxidative stress in that the cell initiates the production of proteins, enzymes, and other compounds to restore homeostasis. At the center of the day-to-day biological response to oxidative stress is the Keap1/Nrf2/ARE pathway, which regulates the transcription of many antioxidant genes that preserve cellular homeostasis and detoxification genes that process and eliminate carcinogens and toxins before they can cause damage. The Keap1/Nrf2/ARE pathway plays a major role in health resilience and can be made more robust and responsive by certain dietary factors. Transient activation of Nrf2 by dietary electrophilic phytochemicals can upregulate antioxidant and chemopreventive enzymes in the absence of actual oxidative stress inducers. Priming the Keap1/Nrf2/ARE pathway by upregulating these enzymes prior to oxidative stress or xenobiotic encounter increases cellular fitness to respond more robustly to oxidative assaults without activating more intense inflammatory NFκB-mediated responses. |
format | Online Article Text |
id | pubmed-4179188 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2014 |
publisher | MDPI |
record_format | MEDLINE/PubMed |
spelling | pubmed-41791882014-10-02 Dietary Regulation of Keap1/Nrf2/ARE Pathway: Focus on Plant-Derived Compounds and Trace Minerals Stefanson, Amanda L. Bakovic, Marica Nutrients Review It has become increasingly evident that chronic inflammation underpins the development of many chronic diseases including cancer, cardiovascular disease and type 2 diabetes. Oxidative stress is inherently a biochemical dysregulation of the redox status of the intracellular environment, which under homeostatic conditions is a reducing environment, whereas inflammation is the biological response to oxidative stress in that the cell initiates the production of proteins, enzymes, and other compounds to restore homeostasis. At the center of the day-to-day biological response to oxidative stress is the Keap1/Nrf2/ARE pathway, which regulates the transcription of many antioxidant genes that preserve cellular homeostasis and detoxification genes that process and eliminate carcinogens and toxins before they can cause damage. The Keap1/Nrf2/ARE pathway plays a major role in health resilience and can be made more robust and responsive by certain dietary factors. Transient activation of Nrf2 by dietary electrophilic phytochemicals can upregulate antioxidant and chemopreventive enzymes in the absence of actual oxidative stress inducers. Priming the Keap1/Nrf2/ARE pathway by upregulating these enzymes prior to oxidative stress or xenobiotic encounter increases cellular fitness to respond more robustly to oxidative assaults without activating more intense inflammatory NFκB-mediated responses. MDPI 2014-09-19 /pmc/articles/PMC4179188/ /pubmed/25244368 http://dx.doi.org/10.3390/nu6093777 Text en © 2014 by the authors; licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution license (http://creativecommons.org/licenses/by/3.0/). |
spellingShingle | Review Stefanson, Amanda L. Bakovic, Marica Dietary Regulation of Keap1/Nrf2/ARE Pathway: Focus on Plant-Derived Compounds and Trace Minerals |
title | Dietary Regulation of Keap1/Nrf2/ARE Pathway: Focus on Plant-Derived Compounds and Trace Minerals |
title_full | Dietary Regulation of Keap1/Nrf2/ARE Pathway: Focus on Plant-Derived Compounds and Trace Minerals |
title_fullStr | Dietary Regulation of Keap1/Nrf2/ARE Pathway: Focus on Plant-Derived Compounds and Trace Minerals |
title_full_unstemmed | Dietary Regulation of Keap1/Nrf2/ARE Pathway: Focus on Plant-Derived Compounds and Trace Minerals |
title_short | Dietary Regulation of Keap1/Nrf2/ARE Pathway: Focus on Plant-Derived Compounds and Trace Minerals |
title_sort | dietary regulation of keap1/nrf2/are pathway: focus on plant-derived compounds and trace minerals |
topic | Review |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4179188/ https://www.ncbi.nlm.nih.gov/pubmed/25244368 http://dx.doi.org/10.3390/nu6093777 |
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