PPAR-γ agonists reduce inflammation in macrophages and vascular cells by inhibiting NF-κB and AP-1 signaling pathways, thereby slowing atherosclerosis progression.

PPAR-γ was the first reported to undergo agonist-dependent simulation, which promotes binding to nuclear receptor co-repressor-1 protein (NCoR) and stabilizes association with promoter-bound NF-κB, thereby leading to the transrepression of inflammatory genes in macrophages [86–88]. ... PPAR-γ also reduces vascular smooth muscle cell proliferation, increases monocyte apoptosis, and suppresses metalloproteinase-9 expression in atherotic plaques [91–94].