Abstract:Atherosclerosis (AS), a chronic and aseptic inflammatory process induced by various factors such as lipid deposition and foam cell formation, is the main pathological basis of most cardiovascular diseases. As the major immune cells in AS lesions, macrophages play a key role in all stages of AS. Thus, modulating the activity of macrophages may be an effective way to intervene the progression of AS. In recent years, with the gradual deepening of the research on programmed cell death, the critical roles of programmed cell death of macrophages in the occurrence and outcome of AS have gradually become a hot topic. Programmed cell death of macrophages is a death process mediated by genetically controlled molecular events, and it includes apoptosis, pyroptosis, autophagy, necroptosis, ferroptosis, parthanatos, and among others. In this review, we summarize the fundamental mechanism underlying programmed cell death of macrophages and the advance on the roles of interactions among all forms of programmed cell death in AS, with a view to providing new strategies for the prevention and treatment of AS.