Lipid and inflammation in atherosclerosis

Abstract

Lipids can be a cause of inflammation especially with regards to the development of atherosclerotic plaque and their subsequent rupture that leads to heart attacks and strokes. Here we discuss the role of biomarkers in this process as well as the effects of oxidized LDL on transformation of macrophages into foam cells and their cytotoxic effects. Moreover, we provide evidence of cholesterol crystal formation early in atherosclerosis and triggering the NLRP3 inflammasomes similar to what is known to occur with monosodium urate crystals in gout. These mechanisms eventually lead to the accumulation of free cholesterol in the extracellular space forming a necrotic core within the plaque. The core then expands with the crystallization of cholesterol from a liquid to a solid state piercing the fibrous cap and the intima to trigger systemic inflammation and subsequent rupture.