Monocytes play a critical role in atherogenesis by their inflammatory signals and differentiation into macrophage foam cells through cholesterol accumulation. The seminal finding of high levels of the peroxisome proliferator-activated receptor gamma in macrophage foam cells has opened up the prospect that its ligands, most importantly the thiazolidinedione class of drugs, might directly influence the development of atheromatous lesions. The present review weighs the growing evidence on regulation of both inflammatory responses and cholesterol homeostasis in macrophages by peroxisome proliferator-activated receptor gamma ligands with regard to their overall impact as antiatherogenic agents.
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