https://scholars.lib.ntu.edu.tw/handle/123456789/593943
標題: | Cross-Talk between Mitochondrial Dysfunction-Provoked Oxidative Stress and Aberrant Noncoding RNA Expression in the Pathogenesis and Pathophysiology of SLE | 作者: | Tsai, Chang-Youh SONG-CHOU HSIEH Lu, Cheng-Shiun Wu, Tsai-Hung Liao, Hsien-Tzung CHENG-HAN WU KO-JEN LI YU-MIN KUO Lee, Hui-Ting CHIEH-YU SHEN CHIA-LI YU |
關鍵字: | cross-talk; long noncoding RNA; microRNA; mitochondrial dysfunction; nitrosative stress. exosome; noncoding RNA; oxidative stress; systemic lupus erythematosus | 公開日期: | 19-十月-2019 | 出版社: | MDPI | 卷: | 20 | 期: | 20 | 起(迄)頁: | 5183 | 來源出版物: | International journal of molecular sciences | 摘要: | Systemic lupus erythematosus (SLE) is a prototype of systemic autoimmune disease involving almost every organ. Polygenic predisposition and complicated epigenetic regulations are the upstream factors to elicit its development. Mitochondrial dysfunction-provoked oxidative stress may also play a crucial role in it. Classical epigenetic regulations of gene expression may include DNA methylation/acetylation and histone modification. Recent investigations have revealed that intracellular and extracellular (exosomal) noncoding RNAs (ncRNAs), including microRNAs (miRs), and long noncoding RNAs (lncRNAs), are the key molecules for post-transcriptional regulation of messenger (m)RNA expression. Oxidative and nitrosative stresses originating from mitochondrial dysfunctions could become the pathological biosignatures for increased cell apoptosis/necrosis, nonhyperglycemic metabolic syndrome, multiple neoantigen formation, and immune dysregulation in patients with SLE. Recently, many authors noted that the cross-talk between oxidative stress and ncRNAs can trigger and perpetuate autoimmune reactions in patients with SLE. Intracellular interactions between miR and lncRNAs as well as extracellular exosomal ncRNA communication to and fro between remote cells/tissues via plasma or other body fluids also occur in the body. The urinary exosomal ncRNAs can now represent biosignatures for lupus nephritis. Herein, we'll briefly review and discuss the cross-talk between excessive oxidative/nitrosative stress induced by mitochondrial dysfunction in tissues/cells and ncRNAs, as well as the prospect of antioxidant therapy in patients with SLE. |
URI: | https://scholars.lib.ntu.edu.tw/handle/123456789/593943 | ISSN: | 16616596 | DOI: | 10.3390/ijms20205183 | SDG/關鍵字: | 1 phosphofructokinase; antioxidant; catalase; glutathione peroxidase; glutathione reductase; glyceraldehyde 3 phosphate dehydrogenase; interleukin 1; interleukin 10; interleukin 17; interleukin 2; long untranslated RNA; reactive oxygen metabolite; STAT3 protein; superoxide dismutase; tumor necrosis factor; untranslated RNA; apoptosis; Article; cell activation; cell communication; cell phagocytosis; cytokine production; disorders of mitochondrial functions; DNA methylation; enzyme activity; enzyme deficiency; epigenetics; gene expression; gene locus; gene silencing; genetic code; genetic polymorphism; histone modification; human; immune response; immunomodulation; molecular interaction; molecular mechanics; mRNA expression level; nitrosative stress; nonhuman; oxidative stress; phenotype; promoter region; protein localization; protein phosphorylation; RNA processing; signal transduction; systemic lupus erythematosus; animal; disease predisposition; gene expression regulation; genetic epigenesis; genetic predisposition; genetics; metabolism; mitochondrion; signal transduction; systemic lupus erythematosus; Animals; Disease Susceptibility; Epigenesis, Genetic; Gene Expression Regulation; Gene Silencing; Genetic Predisposition to Disease; Humans; Lupus Erythematosus, Systemic; Mitochondria; Oxidative Stress; RNA, Untranslated; Signal Transduction |
顯示於: | 醫學系 |
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