Fig. 8.

Proposed model of neointimal formation regulated by NLRC5-PPARγ feedback Vascular injury releases growth factor PDGF-BB that can activate NLRC5, which predominantly resides in the nuclei of VSMCs. NACHT domain of NLRC5 binds to ligand-binding domain (LBD) of PPARγ and facilitates PPARγ activity. PPARγ is in turn recruited at the promoter of NLRC5 and drives NLRC5 transcription. NLRC5-PPARγ positive feedback subsequently regulates downstream gene expression including PCNA, Cyclin D1, α-SMA, Myosin, and Calponin, and eventually suppresses VSMC proliferation, migration, and dedifferentiation and retards neointimal formation