FIGURE 12.

C/EBP homologous protein prevents steatohepatitis. Our model proposes that in the pathogenesis of nonalcoholic steatohepatitis nutrient stress, manifest as elevated FFA, activates macrophages in the liver. Macrophage activation results in the UPR and ER stress, presumably due to the increased secretory load of activated macrophages. CHOP is activated downstream of the UPR. Activated macrophages undergo CHOP-dependent apoptosis with the biologic consequence of dampened inflammation. However, in the absence of CHOP, activated macrophages die less and thus persist in the liver with the consequence of enhanced inflammation.