The Role of Macrophages in Atherosclerosis: Pathophysiologic Mechanisms and Treatment Considerations

Atherosclerotic diseases are a leading cause of morbidity and mortality worldwide, despite the recent diagnostic and therapeutic advances. A thorough understanding of the pathophysiologic mechanisms is thus essential to improve the care of affected individuals. Macrophages are crucial mediators of the atherosclerotic cascade, but their role has not been fully elucidated. The two main subtypes, tissue-resident and monocyte-derived macrophages, have distinct functions that contribute to atherosclerosis development or regression. Since polarization of macrophages to an M2 phenotype and induction of macrophage autophagy have been demonstrated to be atheroprotective, targeting these pathways could represent an appealing approach. Interestingly, macrophage receptors could act as drug targets, as seen in recent experimental studies. Last but not least, macrophage-membrane-coated carriers have been investigated with encouraging results.

Automated summary

Atherosclerotic diseases are a major global health issue, and understanding the role of macrophages in the development and regression of atherosclerosis is crucial for improving patient care. Tissue-resident and monocyte-derived macrophages have distinct functions in the atherosclerotic cascade, and targeting pathways such as M2 polarization and macrophage autophagy shows promise in preventing or treating atherosclerosis. Recent experimental studies have also identified macrophage receptors as potential drug targets, and macrophage-membrane-coated carriers have shown promising results as well.