title: The pathogenesis of systemic lupus erythematosus - From the viewpoint of oxidative stress and mitochondrial dysfunction.
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.
authors.affiliation: Division of Allergy, Immunology and Rheumatology, Taipei Mackay Memorial Hospital, Taiwan; Department of Medicine, Mackay Medical College, Taiwan.
authors.forename: Hui-Ting
authors.initials: HT
authors.lastname: Lee
authors.affiliation: Division of Nephrology, Department of Medicine, Taipei Veterans General Hospital, Taiwan; Faculty of Medicine, National Yang-Ming University, Taiwan.
authors.forename: Tsai-Hung
authors.initials: TH
authors.lastname: Wu
authors.affiliation: Faculty of Medicine, National Yang-Ming University, Taiwan; Division of Thoracic Surgery, Feng-Yuan Hospital, Ministry of Health and Welfare, Taiwan.
authors.forename: Chen-Sung
authors.initials: CS
authors.lastname: Lin
authors.affiliation: Division of Allergy, Immunology and Rheumatology, Taipei Mackay Memorial Hospital, Taiwan; Department of Medicine, Mackay Medical College, Taiwan; Mackay Junior College of Medicine, Nursing, and Management, New Taipei City, Taiwan.
authors.forename: Chyou-Shen
authors.initials: CS
authors.lastname: Lee
authors.affiliation: Department of Medicine, Mackay Medical College, Taiwan; Institute of Biochemistry and Molecular Biology, National Yang-Ming University, Taiwan.
authors.forename: Yau-Huei
authors.initials: YH
authors.lastname: Wei
authors.affiliation: Division of Allergy, Immunology, & Rheumatology, Department of Medicine, Taipei Veterans General Hospital, Taiwan; Faculty of Medicine, National Yang-Ming University, Taiwan. Electronic address: cytsai@vghtpe.gov.tw.
authors.forename: Chang-Youh
authors.initials: CY
authors.lastname: Tsai
authors.affiliation: Division of Allergy, Immunology, & Rheumatology, Department of Medicine, Taipei Veterans General Hospital, Taiwan; Faculty of Medicine, National Yang-Ming University, Taiwan. Electronic address: ming0503@ms3.hinet.net.
authors.forename: Deh-Ming
authors.initials: DM
authors.lastname: Chang
mesh_terms: D004734:Energy Metabolism; D006801:Humans; D008180:Lupus Erythematosus, Systemic / Q000473:pathology* / Q000503:physiopathology*; D008928:Mitochondria / Q000378:metabolism* / Q000473:pathology*; D018384:Oxidative Stress; D017382:Reactive Oxygen Species / Q000378:metabolism*
chemical_list: D017382:Reactive Oxygen Species
keywords: NETosis; Pentose phosphate pathway; Reactive oxygen species; Redox reaction; Systemic lupus erythematosus