KEY RESULTS
Inactivation of C674 inhibited the promoter activity and protein
expression of PPARγ, which could be reversed by inhibitors of
calcineurin or NF-κB. Overexpression of PPARγ2 inhibited the phenotypic
modulation of SKI SMCs. Pioglitazone, the activator of PPARγ, blocked
the activation of NFAT/NF-κB, inhibited SMC phenotypic modulation, and
ameliorated angiotensin II-induced aortic aneurysms in SKI mice.