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Nonalcoholic fatty liver disease (NAFLD) represents a spectrum of diseases ranging from simple steatosis to more severe forms of liver injury including nonalcoholic steatohepatitis (NASH), fibrosis, and hepatocellular carcinoma (HCC). In humans, only 20%‐40% of patients with fatty liver progress to NASH, and mice fed a high‐fat diet (HFD) develop fatty liver but are resistant to NASH development. To understand how simple steatosis progresses to NASH, we examined hepatic expression of anti‐inflammatory microRNA‐223 (miR‐223) and found that this miRNA was highly elevated in hepatocytes in HFD‐fed mice and in human NASH samples. Genetic deletion of miR‐223 induced a full spectrum of NAFLD in long‐term HFD‐fed mice including steatosis, inflammation, fibrosis, and HCC. Furthermore, microarray analyses revealed that, compared to wild‐type mice, HFD‐fed miR‐223 knockout (miR‐223KO) mice …