New Methods in Cardiovascular Biology

Inflammatory monocytes and macrophages are innate im-mune cells that promote the growth and complication of atherosclerotic lesions. Once recruited to the arterial wall, mononuclear phagocytes can ingest lipoproteins. Often, the cells produce proinflammatory mediators and differentiate into foam cells. Activated macrophages also elaborate prote-ases that weaken the plaque’s extracellular matrix.1,2 In early-stage atherosclerosis in mice, most plaque macrophages are direct progeny of recruited blood monocytes that originate in the bone marrow and spleen. In advanced disease, monocyte-derived macrophages proliferate locally, a process that con-tributes dominantly to the cell population in mature plaques.3 Hence, in early and in late disease stages, cellular proliferation pivotally promotes expansion of both the systemic and loca