Abstract
Elevated levels of LDL-cholesterol (LDL-C) and triglycerides (TG) represent significant risk factors for atherosclerotic cardiovascular disease (ASCVD). Despite significant advances in medicine in the field of hypolipidemic agents, we are currently unable to achieve the goals in the treatment of dyslipidemia in many patients.
During the last two decades, the molecule ANGPTL3 (angiopoietin-like 3) has been intensively studied, the inactivation of which using monoclonal antibodies, antisense oligonucleotides, etc. represents a new and promising treatment to reduce the plasma concentration of LDL-C and TG. ANGPTL3 is a factor secreted by the liver that inhibits lipoprotein lipase (LPL) and other lipases by forming a complex with the related protein ANGPTL8.
Extensive genetic studies in individuals who carry genetic variants associated with loss-of-function (LOF) of ANGPTL3 have demonstrated an effect on lowering plasma concentrations of LDL-C and TG, but also on reducing the risk of ASKVO. The results of clinical studies in patients with various forms of dyslipidemia are already known, in which inactivation of ANGPTL3 using monoclonal antibodies or antisense oligonucleotides significantly reduced the plasma concentration of LDL-C and TG.
From this point of view, procedures using ANGPTL3 inhibition have a promising therapeutic potential to reduce the plasma concentration of LDL-C and triglycerides in selected groups of patients with dyslipidemia.