ApoB100 Remodeling and Stiffened Cholesteryl Ester Core Raise LDL Aggregation in Familial Hypercholesterolemia Patients.

Patients with familial hypercholesterolemia (FH) exhibit a significant residual cardiovascular risk. A new cardiovascular risk factor is the susceptibility of individual LDL particles to aggregation. This study examined LDL aggregation and its relationship with LDL lipid composition and biophysical properties in patients with FH compared to controls.

Targeting LDL aggregation decreases atherosclerotic lipid burden in a humanized mouse model of familial hypercholesterolemia: Crucial role of ApoB100 conformational stabilization.

Background And Aims: Low-density lipoprotein (LDL) aggregation is nowadays considered a therapeutic target in atherosclerosis. DP3, the retro-enantio version of the sequence Gly-Cys of LRP1, efficiently inhibits LDL aggregation and foam cell in vitro formation. Here, we investigate whether DP3 modulates atherosclerosis in a humanized ApoB100, LDL receptor (LDLR) knockout mice (LdlrhApoB100 Tg) and determine the potential LDL-related underlying mechanisms.

sICAM-1 concentrations are associated with inflammation in contralateral carotid plaque in patients with ischemic stroke.

Background: Atherosclerotic plaques in the internal carotid artery are responsible for more than 15% of ischemic strokes. Carotid F-fluorodeoxyglucose positron emission tomography (F-FDG PET) detects plaque inflammation. Plasma ICAM-1 and LRP1 concentrations have been associated with inflammation in ipsilateral carotid plaque.

Mechanisms modulating foam cell formation in the arterial intima: exploring new therapeutic opportunities in atherosclerosis.

In recent years, the role of macrophages as the primary cell type contributing to foam cell formation and atheroma plaque development has been widely acknowledged. However, it has been long recognized that diffuse intimal thickening (DIM), which precedes the formation of early fatty streaks in humans, primarily consists of lipid-loaded smooth muscle cells (SMCs) and their secreted proteoglycans. Recent studies have further supported the notion that SMCs constitute the majority of foam cells in advanced atherosclerotic plaques.