Figure 1.

Macrophage polarization in atherosclerotic plaques. Low-density lipoprotein (LDL) enters the vascular intima through damaged endothelial cells and is modified into oxidized LDL, which activates endothelial cells to express chemokines and adhesion molecules, recruiting circulating monocytes. Subsequently, monocytes differentiate into macrophages in a local microenvironment rich in growth factors and pro-inflammatory cytokines. Macrophages rapidly recognize and engulf oxidized LDL, transforming into foam cells and accumulating into plaques. Different subsets of macrophages, including pro-inflammatory macrophages (M1, M4) and anti-inflammatory macrophages (M2, M(Hb), Mhem, Mox), have been found in atherosclerotic plaques. The increased number of pro-inflammatory macrophages and decreased number of anti-inflammatory macrophages lead to a series of inflammatory responses and promote atherosclerotic plaque formation, which eventually lead to cardiovascular disease.