Oxidative Stress and Huntington’s Disease: The Good, The Bad, and The Ugly

Redox homeostasis is crucial for proper cellular functions, including receptor tyrosine kinase signaling, protein folding, and xenobiotic detoxification. Under basal conditions, there is a balance between oxidants and antioxidants. This balance facilitates the ability of oxidants, such as reactive o...

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Bibliographic Details
Published inJournal of Huntington's disease Vol. 5; no. 3; pp. 217 - 237
Main Authors Kumar, Amit, Ratan, Rajiv R.
Format Journal Article
LanguageEnglish
Published London, England SAGE Publications 01.10.2016
Subjects
Humans
Huntington Disease - physiopathology
Oxidative Stress - physiology
Oxidative stress
Huntington’s Disease
transcriptional processes
redox changes
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Summary:Redox homeostasis is crucial for proper cellular functions, including receptor tyrosine kinase signaling, protein folding, and xenobiotic detoxification. Under basal conditions, there is a balance between oxidants and antioxidants. This balance facilitates the ability of oxidants, such as reactive oxygen species, to play critical regulatory functions through a direct modification of a small number of amino acids (e.g. cysteine) on signaling proteins. These signaling functions leverage tight spatial, amplitude, and temporal control of oxidant concentrations. However, when oxidants overwhelm the antioxidant capacity, they lead to a harmful condition of oxidative stress. Oxidative stress has long been held to be one of the key players in disease progression for Huntington’s disease (HD). In this review, we will critically review this evidence, drawing some intermediate conclusions, and ultimately provide a framework for thinking about the role of oxidative stress in the pathophysiology of HD.
ISSN:1879-6397
1879-6397
1879-6400
DOI:10.3233/JHD-160205