High-density lipoprotein functionality in systemic lupus erythematosus.
Abstract
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 incre...Continue Reading
References
Atheroprotective reverse cholesterol transport pathway is defective in familial hypercholesterolemia
Haem oxygenase 1 expression is altered in monocytes from patients with systemic lupus erythematosus.
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