Role of dyslipidemia in accelerating inflammation, autoimmunity, and atherosclerosis in systemic lupus erythematosus and other autoimmune diseases.

Dyslipidemia refers to the abnormality of lipid metabolism. The aberrant lipid profiles are usually characterized by elevated plasma levels of low-density lipoprotein cholesterol (LDL-c), total cholesterol (TC), triglycerides (TGs), apoprotein B (ApoB), and decreased level of high-density lipoprotein cholesterol (HDL-c). Dyslipidemia occurs frequently in autoimmune diseases (ADs), such as systemic lupus erythematosus (SLE), rheumatoid arthritis (RA), type-1 diabetes mellitus (T1DM), psoriasis, and inflammatory bowel disease (IBD), and many other diseases. An imbalance in lipid metabolism contributes to accelerated inflammatory responses in addition to promoting the formation of atherosclerosis. Although there have been many studies and reports on the relationship between abnormal lipid metabolism and ADs, it remains uncertain as to whether dyslipidemia has a unique role in promoting the occurrence and development of ADs. Here, we discuss the mechanisms of how dyslipidemia accelerates inflammatory response, autoimmunity, and atherosclerosis at epidemiological, molecular, and cellular levels, and the discussion is mainly conducted with SLE as an example.