Atherosclerosis is a chronic inflammatory disease characterized by the accumulation of macrophages in arterial walls. Recent studies have shown that macrophages in atherosclerotic lesions are not solely derived from circulating monocytes but can also proliferate locally. This study demonstrates that in atherosclerosis, macrophage accumulation is primarily driven by local proliferation rather than monocyte influx. Using a combination of techniques, including BrdU labeling and parabiosis experiments, the researchers found that macrophages in atherosclerotic lesions turnover rapidly, with a significant portion of these cells arising from local proliferation. The study also identified the scavenger receptor SR-A as a key factor in macrophage proliferation within the lesion microenvironment. These findings suggest that local macrophage proliferation is a critical process in atherosclerosis and may represent a therapeutic target for cardiovascular disease. The study highlights the importance of understanding the dynamic interplay between macrophage proliferation and monocyte recruitment in the progression of atherosclerosis. The results indicate that while monocyte recruitment is important in the early stages of atherosclerosis, local macrophage proliferation becomes increasingly significant as the disease progresses. The study also shows that the microenvironment of the lesion plays a crucial role in regulating macrophage proliferation, with factors such as SR-A contributing to this process. Overall, the study provides new insights into the mechanisms underlying atherosclerosis and highlights the potential for targeting local macrophage proliferation as a therapeutic strategy.Atherosclerosis is a chronic inflammatory disease characterized by the accumulation of macrophages in arterial walls. Recent studies have shown that macrophages in atherosclerotic lesions are not solely derived from circulating monocytes but can also proliferate locally. This study demonstrates that in atherosclerosis, macrophage accumulation is primarily driven by local proliferation rather than monocyte influx. Using a combination of techniques, including BrdU labeling and parabiosis experiments, the researchers found that macrophages in atherosclerotic lesions turnover rapidly, with a significant portion of these cells arising from local proliferation. The study also identified the scavenger receptor SR-A as a key factor in macrophage proliferation within the lesion microenvironment. These findings suggest that local macrophage proliferation is a critical process in atherosclerosis and may represent a therapeutic target for cardiovascular disease. The study highlights the importance of understanding the dynamic interplay between macrophage proliferation and monocyte recruitment in the progression of atherosclerosis. The results indicate that while monocyte recruitment is important in the early stages of atherosclerosis, local macrophage proliferation becomes increasingly significant as the disease progresses. The study also shows that the microenvironment of the lesion plays a crucial role in regulating macrophage proliferation, with factors such as SR-A contributing to this process. Overall, the study provides new insights into the mechanisms underlying atherosclerosis and highlights the potential for targeting local macrophage proliferation as a therapeutic strategy.