Cholesterol metabolism in macrophages

Disturbance of lipid metabolism can lead to the development of pathological processes. Atherosclerosis is a chronic disease characterized by the development of atherosclerotic lesions as a result of the lipid accumulation in the great arterial walls. As a result of cholesterol accumulation by macrophage within the atherosclerotic lesions, they differentiate into foam cells. Macrophage lipid uptake may occur either though the receptor-dependent pathway by low-density lipoprotein receptors and the SR-A, CD36 and LOX-1 scavenger receptors, or the receptor-independent pathway by pinocytosis and phagocytosis. Various enzymes such as ACAT-1 and Abstract    NCEH, enzymes of the biosynthesis and fatty acid oxidation pathways, as well as various transcription factors - SREBP, Nrf1 and Nrf2 participate in the intracellular regulation of lipids. High-density lipoproteins and transporters such as ABCA1, ABCG1 and SR-BI play a vital role in the regulation of cholesterol efflux from cells. Players of lipid metabolism are regulated by various kinase signaling pathways that activate many transcription factors - LXR, RXR, PPARy, NF-kB, etc. Regulation disturbance of intracellular metabolism and imbalance in uptake and efflux of cholesterol from macrophages lead to their differentiation into foam cells. The aim of this review is to describe the mechanisms underlaying lipid metabolism in macrophages and resulting in the transformation of these cells into foam cells.

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