Molecular and Cellular Bases of Immunosenescence, Inflammation, and Cardiovascular Complications Mimicking "Inflammaging" in Patients with Systemic Lupus Erythematosus
Journal
International journal of molecular sciences
Journal Volume
20
Journal Issue
16
Pages
3878
Date Issued
2019-08-09
Author(s)
Tsai, Chang-Youh
Liao, Hsien-Tzung
Lee, Hui-Ting
Lu, Cheng-Shiun
Abstract
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.
Subjects
advanced glycation end product; bioenergetics; immunometabolism; immunosenescence; inflammaging; nitrosative stress; oxidative stress; systemic lupus erythematosus
SDGs
Other Subjects
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
Publisher
MDPI
Type
review