The pathogenesis of systemic lupus erythematosus - From the viewpoint of oxidative stress and mitochondrial dysfunction

SLE is characterized by an increased production of detrimental autoantigens, exaggerated effects of pro-inflammatory cytokines, dysregulated functioning of immunocompetent cells including lymphocytes and leukocytes, and devastating tissue and organ damage. All of these derangements can be potentiate...

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Bibliographic Details
Published in:Mitochondrion 2016-09, Vol.30, p.1-7
Main Authors: Lee, Hui-Ting, Wu, Tsai-Hung, Lin, Chen-Sung, Lee, Chyou-Shen, Wei, Yau-Huei, Tsai, Chang-Youh, Chang, Deh-Ming
Format: Article
Language:English
Subjects:
Energy Metabolism
Humans
Lupus Erythematosus, Systemic - pathology
Lupus Erythematosus, Systemic - physiopathology
Mitochondria - metabolism
Mitochondria - pathology
Oxidative Stress
Reactive Oxygen Species - metabolism
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Summary:SLE is characterized by an increased production of detrimental autoantigens, exaggerated effects of pro-inflammatory cytokines, dysregulated functioning of immunocompetent cells including lymphocytes and leukocytes, and devastating tissue and organ damage. All of these derangements can be potentiated or attenuated by the abnormal energy expenditure and overproduction of reactive oxygen species (ROS). Mitochondrial heteroplasmy or dysfunction has been recognized to play a role in these abnormalities. Abnormal redox reaction, decreased functioning of biogenesis-related enzymes, increased NETosis, harmful cytokine effects, and aberrant lymphocyte behavior have been shown to be associated with the pathological state of mitochondria. There is accumulating data which support the importance of abnormal oxygen metabolism and mitochondrial disorders in the immunopathogenesis of SLE. Further laboratory as well as clinical data are required to expand our understanding of SLE pathogenesis.
ISSN:1567-7249
1872-8278
DOI:10.1016/j.mito.2016.05.007