Fig. 8

Scheme of Cav-1 inhibiting the development of NAFLD by regulating iron metabolism. The HFD inhibited the expression of Cav-1 in hepatocytes and up-regulated the expression of Cav-1 in liver macrophages. In hepatocytes, Cav-1 regulated the FTL/FTH signaling pathway to promote the conversion of Fe²⁺ to Fe³⁺, which helped to slow down the oxidative stress induced by Fe²⁺ and ultimately alleviate the progression of NAFLD. In macrophages, Cav-1 regulated the expression of HO-1 in CD68⁺CD163⁺ macrophages, and promoted the degradation of red blood cells into Fe²⁺ within macrophages which ultimately exacerbated the disorder of iron metabolism in the liver. In addition, the concentration of ferritin and transferrin in serum was up-regulated by Cav-1, and the two were positively correlated in human subject. HFD high-fat diet, Cav-1 caveolin-1, Tf transferrin, NAFLD non-alcoholic fatty liver disease, HO-1 heme oxygenase-1, FTL ferritin light chain, FTH ferritin heavy chain, RBC red blood cell, ROS reactive oxygen species