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SMC heterogeneity in atherosclerosis leaves clinical targeting premature; extends developmental insights for future mechanistic studies.
Smooth muscle cells (SMC) of the vascular system forman intriguing population of cells that are relevant for maintaining vascular tone and function. They also play a key role in pathological processes in the vessel wall. If we focus on the development of intimal thickening in the latter function, it is clear that even this pathological subset presents itself in various forms. That is, arteriosclerosis after hypertension,1 atherosclerosis,2 and restenosis after percuta-neous transluminal coronary angioplasty or coronary artery bypass grafting surgery3 have features in common as well as characteristics selective for each disease. Relevant to an understanding of the above processes is the basic question of whether we are dealing either with a SMC heterogeneity in origin or with a spatiotemporal heterogeneity in expression of differentiation markers. To add to this complexity there is an increasing evidence that already
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Groot et al. (1999) studied this question.
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