FIG. 3.

The working hypothesis of HB-EGF in metabolic disease development. Oxidants produced by the oxidative stress increased HB-EGF expression in the sinusoidal endothelial cells in the liver and bone marrow, causing increases in hepatic VLDL secretion and myeloid cell production. The bone marrow-derived monocytes can be recruited into the subendothelial space of the liver sinusoids and vessel endothelium for the development of inflammation in the liver and vessels. HB-EGF targeting would downregulate the hepatic VLDL production and reduction of the myeloid cell production. FFA, free fatty acid; HSPC, hematopoietic stem and progenitor cell; Mφ, macrophage; MO, monocyte; MPC, myeloid progenitor cell. Color images are available online.