Abstract
Atherosclerosis is a chronic inflammatory disease that contributes to cardiovascular conditions, including coronary artery disease and stroke. Macrophages are central to its pathogenesis, accumulating in arterial walls, engulfing oxidized low-density lipoprotein (oxLDL), and forming foam cells that exacerbate inflammation. These macrophages can polarize into two main subsets: M1 macrophages, which promote inflammation, and M2 macrophages, which resolve inflammation and support tissue repair. The balance between these subsets is crucial for plaque progression and stability. Recent studies have elucidated the immune regulatory functions of macrophages in modulating atherosclerotic plaque formation and vulnerability. Understanding the mechanisms governing macrophage activation, polarization, and immune interactions presents promising therapeutic targets aimed at stabilizing plaques and preventing cardiovascular events. This review summarizes current research on the role of macrophages in atherosclerosis and discusses potential therapies targeting macrophage immune regulation.