Several lines of evidence suggest a biological role for peroxisome proliferator-activated
receptor (PPARδ) in the pathogenesis of atherosclerosis. Administration of synthetic PPARδ
agonists to obese rhesus monkeys elevates serum high-density lipoprotein (HDL)
cholesterol as a result of increased reverse cholesterol transport whilst in vitro studies have
suggested a role for PPARδ in lipid uptake into macrophages. Recent studies have found
that PPARδ depletion from macrophages in LDL receptor (LDLR−/−) mice decreases lesion …