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

Hui Ting Lee, Tsai Hung Wu, Chen Sung Lin, Chyou Shen Lee, Yau Huei Wei, Chang Youh Tsai*, Deh Ming Chang

*Corresponding author for this work

Research output: Contribution to journalReview articlepeer-review

56 Scopus citations

Abstract

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.

Original languageEnglish
Pages (from-to)1-7
Number of pages7
JournalMitochondrion
Volume30
DOIs
StatePublished - 01 09 2016
Externally publishedYes

Bibliographical note

Publisher Copyright:
© 2016 Elsevier B.V. and Mitochondria Research Society.

Keywords

  • NETosis
  • Pentose phosphate pathway
  • Reactive oxygen species
  • Redox reaction
  • Systemic lupus erythematosus

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