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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.

Titel:	Molecular and Cellular Bases of Immunosenescence, Inflammation, and Cardiovascular Complications Mimicking "Inflammaging" in Patients with Systemic Lupus Erythematosus.
Autor/in / Beteiligte Person:	Tsai, CY ; Shen, CY ; Liao, HT ; Li, KJ ; Lee, HT ; Lu, CS ; Wu, CH ; Kuo, YM ; Hsieh, SC ; Yu, CL
Link:	Full Text Finder (Volltext)
Zeitschrift:	International journal of molecular sciences, Jg. 20 (2019-08-09), Heft 16
Veröffentlichung:	Basel, Switzerland : MDPI, [2000-, 2019
Medientyp:	academicJournal
ISSN:	1422-0067 (electronic)
DOI:	10.3390/ijms20163878
Schlagwort:	Animals Cardiovascular Diseases etiology Cardiovascular Diseases metabolism Energy Metabolism Humans Inflammation etiology Inflammation metabolism Lupus Erythematosus, Systemic complications Lupus Erythematosus, Systemic metabolism Metabolome Mitochondria pathology Oxidative Stress Telomere Homeostasis Cardiovascular Diseases pathology Cellular Senescence Inflammation pathology Lupus Erythematosus, Systemic pathology
Sonstiges:	Nachgewiesen in: MEDLINE Sprachen: English Publication Type: Journal Article; Review Language: English [Int J Mol Sci] 2019 Aug 09; Vol. 20 (16). <i>Date of Electronic Publication: </i>2019 Aug 09. MeSH Terms: Cellular Senescence* ; Cardiovascular Diseases / pathology ; Inflammation / pathology ; Lupus Erythematosus, Systemic / *pathology ; Animals ; Cardiovascular Diseases / etiology ; Cardiovascular Diseases / metabolism ; Energy Metabolism ; Humans ; Inflammation / etiology ; Inflammation / metabolism ; Lupus Erythematosus, Systemic / complications ; Lupus Erythematosus, Systemic / metabolism ; Metabolome ; Mitochondria / pathology ; Oxidative Stress ; Telomere Homeostasis References: Cell. 1999 May 14;97(4):419-22. (PMID: 10338204) ; J Exp Med. 1999 Jul 19;190(2):153-6. (PMID: 10432278) ; J Rheumatol. 2001 Feb;28(2):288-91. (PMID: 11246663) ; Clin Immunol. 2001 May;99(2):195-7. (PMID: 11318591) ; Clin Immunol. 2001 May;99(2):211-221. 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Molecular and Cellular Bases of Immunosenescence, Inflammation, and Cardiovascular Complications Mimicking "Inflammaging" in Patients with Systemic Lupus Erythematosus.