Cross-Talk between Mitochondrial Dysfunction-Provoked Oxidative Stress and Aberrant Noncoding RNA Expression in the Pathogenesis and Pathophysiology of SLE.
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.
['Tsai|Chang-Youh|CY|0000-0002-4154-4018', 'Hsieh|Song-Chou|SC|', 'Lu|Cheng-Shiun|CS|0000-0002-4794-9438', 'Wu|Tsai-Hung|TH|', 'Liao|Hsien-Tzung|HT|', 'Wu|Cheng-Han|CH|', 'Li|Ko-Jen|KJ|', 'Kuo|Yu-Min|YM|', 'Lee|Hui-Ting|HT|', 'Shen|Chieh-Yu|CY|', 'Yu|Chia-Li|CL|']
D000818:Animals D004198:Disease Susceptibility D044127:Epigenesis, Genetic D005786:Gene Expression Regulation D020868:Gene Silencing D020022:Genetic Predisposition to Disease D006801:Humans D008180:Lupus Erythematosus, Systemic D008928:Mitochondria D018384:Oxidative Stress D022661:RNA, Untranslated D015398:Signal Transduction
cross-talk oxidative stress noncoding RNA systemic lupus erythematosus microRNA long noncoding RNA mitochondrial dysfunction nitrosative stress. exosome