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The middle layer of the healthy vessel wall, the tunica media, contains an abundant population of vascular smooth muscle cells. During atherosclerosis, lipoproteins and cells accumulate in the tunica intima, which is the innermost layer that separates the media from the lumen. It is widely accepted that the dominant cell populating the atherosclerotic intima is the macrophage, a large myeloid leukocyte known for its proficiency at scavenging just about anything from bacteria to apoptotic cells to oxidized lipoproteins. The development of atherosclerosis, the theory goes, is a story of macrophages accumulating in the vessel wall, eating lipoproteins, becoming foam cells, and wreaking inflammatory and metabolic havoc.1Article, see p 662“Monocytes give rise to macrophages.” This statement, uttered just few years ago, would have been considered a truism. Today, somewhat dismantled, it is being reimagined. In 1968, while examining the relationship between circulating and “fixed” mononuclear phagocytes, van Furth and Cohn posited that “monocytes migrate randomly from the peripheral blood into the tissues, where they are called macrophages.”2 This insight has profoundly influenced our thinking; that lesional macrophages likewise derive from circulating monocytes is much rooted in this tradition. Perhaps then, the recent observations that tissue macrophages in the steady state do not require monocytes were surprising if not entirely unexpected.3–6 In the context of atherosclerosis, could it be that we were wrong all along? Are lesional macrophages derived from something other than monocytes?Enter the vascular smooth muscle cell (VSMC): unlike other smooth muscle cells, VSMCs are …

Do Vascular Smooth Muscle Cells Differentiate to Macrophages in Atherosclerotic Lesions?