Purpose of review: It is well accepted that LDLs and its modified form oxidized-LDL (ox-LDL) play a major role in the development of atherosclerosis and foam cell formation. Whereas the majority of these cells have been demonstrated to be derived from macrophages, smooth muscle cells (SMCs) give rise to a significant number of foam cells as well. During atherosclerotic plaque formation, SMCs switch from a contractile to a synthetic phenotype. The contribution of this process to foam cell formation is still not well understood.
Recent findings: It has been confirmed that a large proportion of foam cells in human atherosclerotic plaques and in experimental intimal thickening arise from SMCs. SMC-derived foam cells express receptors involved in ox-LDL uptake and HDL reverse transport. In-vitro studies show that treatment of SMCs with ox-LDL induces typical foam-cell formation; this process is associated with a transition of SMCs toward a synthetic phenotype.
Summary: This review summarizes data regarding the phenotypic switch of arterial SMCs within atherosclerotic lesion and their contribution to intimal foam cell formation.