Abstract
Nonalcoholic fatty liver disease (NAFLD) is a major health issue. NAFLD can progress from simple hepatic steatosis to nonalcoholic steatohepatitis (NASH). NASH can progress to cirrhosis or hepatocellular carcinoma. Unfortunately, there is no currently approved pharmacologic therapy for NAFLD patients. The six transmembrane protein of prostate 2 (STAMP2), a metalloreductase involved in iron and copper homeostasis, is well known for its critical role in the coordination of glucose/lipid metabolism and inflammation in metabolic tissues. We previously demonstrated that hepatic STAMP2 could be a suitable therapeutic target for NAFLD. In this review, we discuss the emerging role of STAMP2 in the dysregulation of iron metabolism events leading to NAFLD and suggest therapeutic strategies targeting STAMP2.