ApoB100 and Atherosclerosis: What’s New in the 21st Century?

Abstract

ApoB is the main protein of triglyceride-rich lipoproteins and is further divided into ApoB48 in the intestine and ApoB100 in the liver. Very low-density lipoprotein (VLDL) is produced by the liver, contains ApoB100, and is metabolized into its remnants, intermediate-density lipoprotein (IDL) and low-density lipoprotein (LDL). ApoB100 has been suggested to play a crucial role in the formation of the atherogenic plaque. Apart from being a biomarker of atherosclerosis, ApoB100 seems to be implicated in the inflammatory process of atherosclerosis per se. In this review, we will focus on the structure, the metabolism, and the function of ApoB100, as well as its role as a predictor biomarker of cardiovascular risk. Moreover, we will elaborate upon the molecular mechanisms regarding the pathophysiology of atherosclerosis, and we will discuss the disorders associated with the APOB gene mutations, and the potential role of various drugs as therapeutic targets.

Lipoprotein(a) and Atherosclerotic Cardiovascular Disease: Where Do We Stand?

“…Lipoprotein apheresis (LA) is a therapeutic technique designed to selectively remove apoB-containing lipoproteins from the bloodstream, including lipoprotein(a) [ 231 ]. Beyond its primary role in reducing lipoprotein levels, LA has been found to exert various pleiotropic effects that may contribute to its therapeutic benefits.…”

“…LA is typically indicated for individuals with familial hypercholesterolemia (both heterozygous and homozygous) who fail to achieve therapeutic targets despite maximal tolerated lipid-lowering therapy. However, it is worth noting that a rebound phenomenon can occur following LA, with LDL-C and Lp(a) concentrations returning to baseline levels within approximately two weeks after treatment [ 231 ].…”