Atherogenic lipids and macrophage subsets

Macrophage foam cells are important cells in the vascular wall that contribute to the inflammation associated with atherosclerotic lesions. Recent studies have demonstrated the heterogeneity of macrophages in lesions. In this review, advances in our understanding of the formation of foam cells by macrophage subsets in atherosclerotic plaques will be discussed.

Macrophage subsets develop in response to the microenvironment in the arterial wall. The uptake of lipoproteins, particularly oxidized LDL, has been considered the major mechanism of foam cell formation. However, native and aggregated LDL can also be taken up by macrophages and M2 macrophages have been shown to be efficient in the uptake of apoptotic cells that can contribute lipids to the cells. The ability of the macrophage subsets to respond to bioactive lipids in the artery wall to either promote macrophage subset polarization and/or to promote foam cell formation is only beginning to be understood.

Although we are beginning to appreciate the heterogeneity of macrophages present in atherosclerotic plaques, further work is required to fully understand the molecular basis for the differential ability of macrophage subsets to form foam cells and to respond to bioactive lipids.