The iterative lipid impact on inflammation in atherosclerosis

Abstract

Purpose of review Lipid-mediated atherogenesis is hallmarked by a chronic inflammatory state. Low-density lipoprotein cholesterol (LDL-C), triglyceride rich lipoproteins (TRLs), and lipoprotein(a) [Lp(a)] are causally related to atherosclerosis. Within the paradigm of endothelial activation and subendothelial lipid deposition, these lipoproteins induce numerous pro-inflammatory pathways. In this review, we will outline the effects of lipoproteins on systemic inflammatory pathways in atherosclerosis. Recent findings Apolipoprotein B-containing lipoproteins exert a variety of pro-inflammatory effects, ranging from the local artery to systemic immune cell activation. LDL-C, TRLs, and Lp(a) induce endothelial dysfunction with concomitant activation of circulating monocytes through enhanced lipid accumulation. The process of trained immunity of the innate immune system, predominantly induced by LDL-C particles, hallmarks the propagation of the low-grade inflammatory response. In concert, bone marrow activation induces myeloid skewing, further contributing to immune cell mobilization and plaque progression. Summary Lipoproteins and inflammation are intertwined in atherogenesis. Elucidating the inflammatory pathways will provide new opportunities for therapeutic agents.