High-density lipoprotein functionality in systemic lupus erythematosus
| Autor: | Leila Shirmohammadi, Shiva Ganjali, Amirhossein Sahebkar, Morgayn I. Read |
|---|---|
| Rok vydání: | 2020 |
| Předmět: |
Endothelial lipase
Very low-density lipoprotein Endothelium Inflammation Pathogenesis Mice 03 medical and health sciences chemistry.chemical_compound 0302 clinical medicine High-density lipoprotein Rheumatology Risk Factors medicine Animals Humans Lupus Erythematosus Systemic 030212 general & internal medicine Serum amyloid A Autoantibodies 030203 arthritis & rheumatology Apolipoprotein A-I business.industry Atherosclerosis Anesthesiology and Pain Medicine medicine.anatomical_structure chemistry Immunology lipids (amino acids peptides and proteins) medicine.symptom Lipoproteins HDL business Lipoprotein |
| Zdroj: | Seminars in Arthritis and Rheumatism. 50:769-775 |
| ISSN: | 0049-0172 |
| Popis: | Systemic lupus erythematosus (SLE) is a heterogeneous disease which is characterized with excessive inflammation and autoantibodies, macrophage and complement activation, and subsequently immunologically mediated tissue damage. In spite of improved treatments of SLE, these patients experience premature atherosclerosis and the rate of mortality among them remains high. Autoantibodies and circulating immune complexes might contribute to the pathogenesis of atherosclerosis by injuring the endothelium, as well as inducing pro-inflammatory and pro-adhesive endothelial cell phenotypes, as well as altering the metabolism of lipoproteins involved in atherogenesis. Hence, high levels of atherogenic lipoproteins (like low-density lipoprotein (LDL) and very low-density lipoprotein (VLDL)) and low levels of high-density lipoprotein (HDL-C) are important risk factors for atherosclerotic cardiovascular complications in SLE patients but these traditional risk factors fail to fully explain the increased risk of cardiovascular disease (CVD) in these patients. The exact mechanism by which inflammation decreases HDL levels is not defined, but decreases in apoA-I production and lecithin cholesterol acyltransferase (LCAT) activity, as well as increased serum amyloid A (SAA), endothelial lipase and secretory phospholipase A2 activity (PLA2) could all contribute. In addition, during inflammation multiple changes in HDL structure occur, leading to alterations in HDL function which may be implicated in the CVD complications of SLE. Therefore, this review will aim to identify the mechanisms implicated in HDL dysfunction which occurs in SLE patients. |
| Databáze: | OpenAIRE |
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