Molecular and Cellular Bases of Immunosenescence, Inflammation, and Cardiovascular Complications Mimicking “Inflammaging” in Patients with Systemic Lupus Erythematosus

• Published in: International journal of molecular sciences Vol. 20; no. 16; p. 3878
• Main Authors: Tsai, Chang-Youh, Shen, Chieh-Yu, Liao, Hsien-Tzung, Li, Ko-Jen, Lee, Hui-Ting, Lu, Cheng-Shiun, Wu, Cheng-Han, Kuo, Yu-Min, Hsieh, Song-Chou, Yu, Chia-Li
• Format: Journal Article
• Language: English
• Published: Switzerland MDPI AG 09.08.2019; MDPI
• Subjects: Aging; Animals; Antigens; Apoptosis; Bioenergetics; Biomarkers; Bone marrow; Cardiovascular Diseases - etiology; Cardiovascular Diseases - metabolism; Cardiovascular Diseases - pathology; Cellular Senescence; Cytokines; Deoxyribonucleic acid; DNA; DNA damage; Energy Metabolism; Enzymes; Glycoproteins; Humans; Inflammation; Inflammation - etiology; Inflammation - metabolism; Inflammation - pathology; Lipids; Lupus; Lupus Erythematosus, Systemic - complications; Lupus Erythematosus, Systemic - metabolism; Lupus Erythematosus, Systemic - pathology; Lymphocytes; Memory; Metabolic syndrome; Metabolome; Mitochondria - pathology; Mitochondrial DNA; Older people; Oxidation; Oxidative Stress; Proteins; Review; Senescence; Stem cells; Telomerase; Telomere Homeostasis; advanced glycation end product; immunosenescence; inflammaging; nitrosative stress; systemic lupus erythematosus; bioenergetics; immunometabolism; oxidative stress
• ISSN: 1422-0067; 1661-6596; 1422-0067
• DOI: 10.3390/ijms20163878

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.