CD36: linking lipids to the NLRP3 inflammasome, atherogenesis and atherothrombosis

Abstract

A recent study published in Nature Immunology by Sheedy et al.1 indicates that uptake of modified low-density lipoprotein (LDL) by the scavenger receptor CD36 primes and activates the NLRP3 inflammasome, providing an early pathogenic pathway that links cholesterol accumulation to the chronic inflammatory process of atherosclerosis.1 Atherosclerosis arises from chronic vascular inflammation elicited by lipids. During the past few years, several studies have sought to identify the mechanistic link between lipids and inflammation in atherogenesis. Foam cell formation involves the phagocytosis of matrix-retained lipoproteins and the fluid-phase pinocytosis of aggregated lipoproteins by macrophages; however, a substantial body of evidence also suggests that oxidative modification of subendothelially accumulated LDL triggers the inflammatory process underlying atherosclerosis.