https://scholars.lib.ntu.edu.tw/handle/123456789/593944
標題: | Molecular and Cellular Bases of Immunosenescence, Inflammation, and Cardiovascular Complications Mimicking "Inflammaging" in Patients with Systemic Lupus Erythematosus | 作者: | Tsai, Chang-Youh CHIEH-YU SHEN Liao, Hsien-Tzung KO-JEN LI Lee, Hui-Ting Lu, Cheng-Shiun CHENG-HAN WU YU-MIN KUO SONG-CHOU HSIEH CHIA-LI YU |
關鍵字: | advanced glycation end product; bioenergetics; immunometabolism; immunosenescence; inflammaging; nitrosative stress; oxidative stress; systemic lupus erythematosus | 公開日期: | 9-八月-2019 | 出版社: | MDPI | 卷: | 20 | 期: | 16 | 起(迄)頁: | 3878 | 來源出版物: | International journal of molecular sciences | 摘要: | Systemic lupus erythematosus (SLE) is an archetype of systemic autoimmune disease, characterized by the presence of diverse autoantibodies and chronic inflammation. There are multiple factors involved in lupus pathogenesis, including genetic/epigenetic predisposition, sexual hormone imbalance, environmental stimulants, mental/psychological stresses, and undefined events. Recently, many authors noted that "inflammaging", consisting of immunosenescence and inflammation, is a common feature in aging people and patients with SLE. It is conceivable that chronic oxidative stresses originating from mitochondrial dysfunction, defective bioenergetics, abnormal immunometabolism, and premature telomere erosion may accelerate immune cell senescence in patients with SLE. The mitochondrial dysfunctions in SLE have been extensively investigated in recent years. The molecular basis of normoglycemic metabolic syndrome has been found to be relevant to the production of advanced glycosylated and nitrosative end products. Besides, immunosenescence, autoimmunity, endothelial cell damage, and decreased tissue regeneration could be the results of premature telomere erosion in patients with SLE. Herein, the molecular and cellular bases of inflammaging and cardiovascular complications in SLE patients will be extensively reviewed from the aspects of mitochondrial dysfunctions, abnormal bioenergetics/immunometabolism, and telomere/telomerase disequilibrium. |
URI: | https://scholars.lib.ntu.edu.tw/handle/123456789/593944 | ISSN: | 16616596 | DOI: | 10.3390/ijms20163878 | SDG/關鍵字: | advanced glycation end product; alpha interferon; autoantigen; caspase 10; caspase 9; CD28 antigen; gamma interferon; gamma interferon inducible protein 10; glutathione; granzyme B; high density lipoprotein; interleukin 10; interleukin 17; interleukin 22; interleukin 23; interleukin 6; low density lipoprotein; mammalian target of rapamycin; monocyte chemotactic protein 1; perforin; reactive nitrogen species; reactive oxygen metabolite; telomerase; transforming growth factor beta; very low density lipoprotein; aging; apoptosis; autoimmunity; autophagy; bioenergy; cardiovascular disease; CD4+ T lymphocyte; cytokine production; disease predisposition; DNA damage; glycolysis; glycosylation; histone modification; human; immunosenescence; inflammaging; inflammation; lipid peroxidation; metabolic syndrome X; metabolomics; mitochondrial dynamics; mitochondrial respiration; mitophagy; morbidity; nitrosative stress; nonhuman; oxidative phosphorylation; oxidative stress; protein expression; protein processing; Review; systemic lupus erythematosus; T lymphocyte activation; telomere homeostasis; animal; cardiovascular disease; cell aging; complication; energy metabolism; inflammation; metabolism; metabolome; mitochondrion; pathology; systemic lupus erythematosus; Animals; Cardiovascular Diseases; Cellular Senescence; Energy Metabolism; Humans; Inflammation; Lupus Erythematosus, Systemic; Metabolome; Mitochondria; Oxidative Stress; Telomere Homeostasis |
顯示於: | 醫學系 |
在 IR 系統中的文件,除了特別指名其著作權條款之外,均受到著作權保護,並且保留所有的權利。