A Mitochondria-Associated Oxidative Stress Perspective on Huntington’s Disease

Huntington’s disease (HD) is genetically caused by mutation of the Huntingtin (HTT) gene. At present, the mechanisms underlying the defect of HTT and the development of HD remain largely unclear. However, increasing evidence shows the presence of enhanced oxidative stress in HD patients. In this rev...

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Autores principales: Zheng, Ju, Winderickx, Joris, Franssens, Vanessa, Liu, Beidong
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Frontiers Media S.A. 2018
Materias:
Neuroscience
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6156126/
https://www.ncbi.nlm.nih.gov/pubmed/30283298
http://dx.doi.org/10.3389/fnmol.2018.00329
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author Zheng, Ju
Winderickx, Joris
Franssens, Vanessa
Liu, Beidong
author_facet Zheng, Ju
Winderickx, Joris
Franssens, Vanessa
Liu, Beidong
author_sort Zheng, Ju
collection PubMed
description Huntington’s disease (HD) is genetically caused by mutation of the Huntingtin (HTT) gene. At present, the mechanisms underlying the defect of HTT and the development of HD remain largely unclear. However, increasing evidence shows the presence of enhanced oxidative stress in HD patients. In this review article, we focus on the role of oxidative stress in the pathogenesis of HD and discuss mediators and potential mechanisms involved in mutant HTT-mediated oxidative stress generation and progression. Furthermore, we emphasize the role of the unicellular organism Saccharomyces cerevisiae in investigating mutant HTT-induced oxidative stress. Overall, this review article provides an overview of the latest findings regarding oxidative stress in HD and potential therapeutic targets for HD.
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spelling pubmed-61561262018-10-03 A Mitochondria-Associated Oxidative Stress Perspective on Huntington’s Disease Zheng, Ju Winderickx, Joris Franssens, Vanessa Liu, Beidong Front Mol Neurosci Neuroscience Huntington’s disease (HD) is genetically caused by mutation of the Huntingtin (HTT) gene. At present, the mechanisms underlying the defect of HTT and the development of HD remain largely unclear. However, increasing evidence shows the presence of enhanced oxidative stress in HD patients. In this review article, we focus on the role of oxidative stress in the pathogenesis of HD and discuss mediators and potential mechanisms involved in mutant HTT-mediated oxidative stress generation and progression. Furthermore, we emphasize the role of the unicellular organism Saccharomyces cerevisiae in investigating mutant HTT-induced oxidative stress. Overall, this review article provides an overview of the latest findings regarding oxidative stress in HD and potential therapeutic targets for HD. Frontiers Media S.A. 2018-09-19 /pmc/articles/PMC6156126/ /pubmed/30283298 http://dx.doi.org/10.3389/fnmol.2018.00329 Text en Copyright © 2018 Zheng, Winderickx, Franssens and Liu. http://creativecommons.org/licenses/by/4.0/ This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
spellingShingle Neuroscience
Zheng, Ju
Winderickx, Joris
Franssens, Vanessa
Liu, Beidong
A Mitochondria-Associated Oxidative Stress Perspective on Huntington’s Disease
title A Mitochondria-Associated Oxidative Stress Perspective on Huntington’s Disease
title_full A Mitochondria-Associated Oxidative Stress Perspective on Huntington’s Disease
title_fullStr A Mitochondria-Associated Oxidative Stress Perspective on Huntington’s Disease
title_full_unstemmed A Mitochondria-Associated Oxidative Stress Perspective on Huntington’s Disease
title_short A Mitochondria-Associated Oxidative Stress Perspective on Huntington’s Disease
title_sort mitochondria-associated oxidative stress perspective on huntington’s disease
topic Neuroscience
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6156126/
https://www.ncbi.nlm.nih.gov/pubmed/30283298
http://dx.doi.org/10.3389/fnmol.2018.00329
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