NR2C2 and atherosclerosis: However, Xie et al. [23] found PPAR ligands/activators such as the PUFA metabolites, 15-HETE and 13-HODE, could trans-activate TR4, and some TZDs could also trans-activate TR4 to modulate its down-stream target CD36 activity during foam cell formation/atherosclerosis [39].