期刊
INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
卷 20, 期 16, 页码 -出版社
MDPI
DOI: 10.3390/ijms20163878
关键词
systemic lupus erythematosus; immunosenescence; inflammaging; oxidative stress; nitrosative stress; bioenergetics; immunometabolism; advanced glycation end product
资金
- Ministry of Science and Technology, Taiwan [MOST-107-2314-B-075-051-MY3]
- Taipen Veterans General Hospital, Taiwan [V108C-203, v107D37-002-MY3]
- Executive Yuan, Taiwan
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.
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