Hepatic–vascular crosstalk via GRK2: fenofibrate improves endothelial function by restoring lipid metabolism and NO signaling in obese mice

Fenofibrate improves endothelial-dependent relaxation and NO production in HFD-induced obese mice, likely through activation of the LKB1/AMPK/Akt pathway. The suppression of hepatic GRK2 activity by fenofibrate may contribute to better lipid metabolism, thereby promoting the recovery of vascular function.