کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
8398940 | 1544414 | 2016 | 39 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
The pathogenesis of systemic lupus erythematosus - From the viewpoint of oxidative stress and mitochondrial dysfunction
ترجمه فارسی عنوان
پاتوژنز لوپوس اریتماتوز سیستمیک - از دیدگاه استرس اکسیداتیو و اختلال عملکرد میتوکندریال
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کلمات کلیدی
موضوعات مرتبط
علوم زیستی و بیوفناوری
بیوشیمی، ژنتیک و زیست شناسی مولکولی
بیوفیزیک
چکیده انگلیسی
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.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Mitochondrion - Volume 30, September 2016, Pages 1-7
Journal: Mitochondrion - Volume 30, September 2016, Pages 1-7
نویسندگان
Hui-Ting Lee, Tsai-Hung Wu, Chen-Sung Lin, Chyou-Shen Lee, Yau-Huei Wei, Chang-Youh Tsai, Deh-Ming Chang,