This review summarizes current therapeutic targets for dyslipidemia, focusing on raising HDL-C via endothelial lipase, LCAT, and apoAI, and lowering LDL-C via PCSK9, MTP, and apoB mRNA.
This review summarizes current and emerging therapeutic targets for managing dyslipidemia to prevent atherosclerosis.
Maintaining cholesterol and triglyceride (TG) levels within healthy limits is critical for decreasing the risk of heart disease. Dyslipidemia refers to the abnormal levels of lipids in the blood, including low high-density lipoprotein cholesterol (HDL-C), also known as good cholesterol, high low-density lipoprotein cholesterol (LDL-C), also known as bad cholesterol, and/or high TG levels that contribute to the development and progression of atherosclerosis. In this article we reviewed some of the current therapeutic targets for the treatment of dyslipidemia, with a primary focus on endothelial lipase and lecithin cholesterol acyl transferase for raising HDL-C, and the proprotein convertase subtilisin-like kexin type 9 (PCSK9), microsomal triglyceride transfer protein, and the messenger RNA of apolipoprotein B for lowering LDL-C. In addition, we reviewed the role of apolipoprotein AI (apoAI) in raising HDL-C, where we discuss three apoAI-based drugs under development. These are its mutated dimer (apoAI-Milano), a complex with phospholipids, and a mimetic peptide. Atherosclerosis, mainly because of dyslipidemia, is a leading cause of cardiovascular disease. Regarding the title of this article, the 'good' refers to HDL-C, the 'bad' refers to LDL-C, and the 'ugly' refers to atherosclerosis.
Elshourbagy et al. (Wed,) conducted a review in Dyslipidemia. Therapeutic targets for dyslipidemia (endothelial lipase, LCAT, PCSK9, MTP, apoB mRNA, apoAI) was evaluated. This review summarizes current therapeutic targets for dyslipidemia, focusing on raising HDL-C via endothelial lipase, LCAT, and apoAI, and lowering LDL-C via PCSK9, MTP, and apoB mRNA.