N-(carboxymethyl)lysine promotes lipid uptake of macrophage cluster of differentiation 36 and receptor for advanced glycation end products.

Background: Advanced glycation end products (AGEs) are diabetic metabolic toxic products that cannot be ignored. N-(carboxymethyl)lysine (CML), a component of AGEs, could increase macrophage lipid uptake, promote foam cell formation, and thereby accelerate atherosclerosis. The receptor for AGEs (RAGE) and cluster of differentiation 36 (CD36) were the receptors of CML.

[Bioinformatics analysis identifies aging/senescence-induced genes in calcified plaques].

Vascular calcification is an important pathophysiological basis of cardiovascular disease with its underlying mechanism unclear. In recent years, studies have shown that aging is one of the risk factors for vascular calcification. The purpose of this study was to investigate the microenvironmental characteristics of vascular calcification, identify aging/senescence-induced genes (ASIGs) closely related to calcified plaques, and explore the evolution trajectory of vascular calcification cell subsets.