Molecular and Cellular Bases of Immunosenescence, Inflammation, and Cardiovascular Complications Mimicking “Inflammaging” in Patients with Systemic Lupus Erythematosus
Division of Allergy, Immunology & Rheumatology, Taipei Veterans General Hospital & National Yang-Ming University, #201 Sec 2, Shih-Pai Road, Taipei 11217, Taiwan
Institute of Clinical Medicine, National Taiwan University College of Medicine, #7 Chung-Shan South Road, Taipei 10002, Taiwan
Department of Internal Medicine, National Taiwan University Hospital, #7 Chung-Shan South Road, Taipei 10002, Taiwan
Section of Allergy, Immunology & Rheumatology, MacKay Memorial Hospital, #92 Section 2, Chung-Shan North Road, Taipei 10449, Taiwan
Author to whom correspondence should be addressed.
Int. J. Mol. Sci. 2019, 20(16), 3878; https://doi.org/10.3390/ijms20163878
Received: 15 July 2019 / Revised: 4 August 2019 / Accepted: 5 August 2019 / Published: 9 August 2019
(This article belongs to the Special Issue Systemic Lupus Erythematosus: Research Updates in Immunopathogenesis, Biomarkers and Therapeutics)
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.