1. Hepatic inflammation and fibrosis: Functional links and key pathways.

    Hepatology 61(3):1066 (2015) PMID 25066777 PMCID PMC4306641

    Inflammation is one of the most characteristic features of chronic liver disease of viral, alcoholic, fatty, and autoimmune origin. Inflammation is typically present in all disease stages and associated with the development of fibrosis, cirrhosis, and hepatocellular carcinoma. In the past decade...
  2. Effect of weight loss on magnetic resonance imaging estimation of liver fat and volume in patients with nonalcoholic steatohepatitis.

    Clinical Gastroenterology and Hepatology 13(3):561 (2015) PMID 25218667 PMCID PMC4333065

    Little is known about how weight loss affects magnetic resonance imaging (MRI) of liver fat and volume or liver histology in patients with nonalcoholic steatohepatitis (NASH). We measured changes in liver fat and liver volume associated with weight loss by using an advanced MRI method. We analyz...
  3. Effect of weight loss on magnetic resonance imaging estimation of liver fat and volume in patients with nonalcoholic steatohepatitis.

    Clinical Gastroenterology and Hepatology 13(3):561 (2015) PMID 25218667

    Little is known about how weight loss affects magnetic resonance imaging (MRI) of liver fat and volume or liver histology in patients with nonalcoholic steatohepatitis (NASH). We measured changes in liver fat and liver volume associated with weight loss by using an advanced MRI method. We analyz...
  4. Effect of weight loss on magnetic resonance imaging estimation of liver fat and volume in patients with nonalcoholic steatohepatitis.

    Clinical Gastroenterology and Hepatology 13(3):561 (2015) PMID 25218667

    Little is known about how weight loss affects magnetic resonance imaging (MRI) of liver fat and volume or liver histology in patients with nonalcoholic steatohepatitis (NASH). We measured changes in liver fat and liver volume associated with weight loss by using an advanced MRI method. We analyz...
  5. Effect of weight loss on magnetic resonance imaging estimation of liver fat and volume in patients with nonalcoholic steatohepatitis.

    Clinical Gastroenterology and Hepatology 13(3):561 (2015) PMID 25218667

    Little is known about how weight loss affects magnetic resonance imaging (MRI) of liver fat and volume or liver histology in patients with nonalcoholic steatohepatitis (NASH). We measured changes in liver fat and liver volume associated with weight loss by using an advanced MRI method. We analyz...
  6. Hepatic inflammation and fibrosis: Functional links and key pathways.

    Hepatology 61(3):1066 (2015) PMID 25066777

    Inflammation is one of the most characteristic features of chronic liver disease of viral, alcoholic, fatty, and autoimmune origin. Inflammation is typically present in all disease stages and associated with the development of fibrosis, cirrhosis, and hepatocellular carcinoma. In the past decade...
  7. Hepatic inflammation and fibrosis: Functional links and key pathways.

    Hepatology 61(3):1066 (2015) PMID 25066777 PMCID PMC4306641

    Inflammation is one of the most characteristic features of chronic liver disease of viral, alcoholic, fatty, and autoimmune origin. Inflammation is typically present in all disease stages and associated with the development of fibrosis, cirrhosis, and hepatocellular carcinoma. In the past decade...
  8. The TM6SF2 variants, novel genetic predictors for nonalcoholic steatohepatitis.

    Gastroenterology 148(1):252 (2015) PMID 25451657

  9. ER Stress Cooperates with Hypernutrition to Trigger TNF-Dependent Spontaneous HCC Development

    Cancer Cell 26(3):331 (2014)

    Endoplasmic reticulum (ER) stress has been implicated in the pathogenesis of viral hepatitis, insulin resistance, hepatosteatosis, and nonalcoholic steatohepatitis (NASH), disorders that increase risk of hepatocellular carcinoma (HCC). To determine whether and how ER stress contributes...
  10. ER stress cooperates with hypernutrition to trigger TNF-dependent spontaneous HCC development.

    Cancer Cell 26(3):331 (2014) PMID 25132496 PMCID PMC4165611

    Endoplasmic reticulum (ER) stress has been implicated in the pathogenesis of viral hepatitis, insulin resistance, hepatosteatosis, and nonalcoholic steatohepatitis (NASH), disorders that increase risk of hepatocellular carcinoma (HCC). To determine whether and how ER stress contributes to obesit...
  11. ER stress cooperates with hypernutrition to trigger TNF-dependent spontaneous HCC development.

    Cancer Cell 26(3):331 (2014) PMID 25132496 PMCID PMC4165611

    Endoplasmic reticulum (ER) stress has been implicated in the pathogenesis of viral hepatitis, insulin resistance, hepatosteatosis, and nonalcoholic steatohepatitis (NASH), disorders that increase risk of hepatocellular carcinoma (HCC). To determine whether and how ER stress contributes to obesit...
  12. Reply: To PMID 23996730.

    Hepatology 60(3):1114 (2014) PMID 24443149 PMCID PMC4328032

  13. Reply: To PMID 23996730.

    Hepatology 60(3):1114 (2014) PMID 24443149 PMCID PMC4328032

  14. Reply: To PMID 23996730.

    Hepatology 60(3):1114 (2014) PMID 24443149

  15. TAK1-mediated autophagy and fatty acid oxidation prevent hepatosteatosis and tumorigenesis.

    Journal of Clinical Investigation 124(8):3566 (2014) PMID 24983318 PMCID PMC4109552

    The MAP kinase kinase kinase TGFβ-activated kinase 1 (TAK1) is activated by TLRs, IL-1, TNF, and TGFβ and in turn activates IKK-NF-κB and JNK, which regulate cell survival, growth, tumorigenesis, and metabolism. TAK1 signaling also upregulates AMPK activity and autophagy. Here, we investigated T...
  16. TAK1-mediated autophagy and fatty acid oxidation prevent hepatosteatosis and tumorigenesis.

    Journal of Clinical Investigation 124(8):3566 (2014) PMID 24983318 PMCID PMC4109552

    The MAP kinase kinase kinase TGFβ-activated kinase 1 (TAK1) is activated by TLRs, IL-1, TNF, and TGFβ and in turn activates IKK-NF-κB and JNK, which regulate cell survival, growth, tumorigenesis, and metabolism. TAK1 signaling also upregulates AMPK activity and autophagy. Here, we investigated T...
  17. TAK1-mediated autophagy and fatty acid oxidation prevent hepatosteatosis and tumorigenesis.

    Journal of Clinical Investigation 124(8):3566 (2014) PMID 24983318 PMCID PMC4109552

    The MAP kinase kinase kinase TGFβ-activated kinase 1 (TAK1) is activated by TLRs, IL-1, TNF, and TGFβ and in turn activates IKK-NF-κB and JNK, which regulate cell survival, growth, tumorigenesis, and metabolism. TAK1 signaling also upregulates AMPK activity and autophagy. Here, we investigated T...
  18. TAK1-mediated autophagy and fatty acid oxidation prevent hepatosteatosis and tumorigenesis.

    Journal of Clinical Investigation 124(8):3566 (2014) PMID 24983318 PMCID PMC4109552

    The MAP kinase kinase kinase TGFβ-activated kinase 1 (TAK1) is activated by TLRs, IL-1, TNF, and TGFβ and in turn activates IKK-NF-κB and JNK, which regulate cell survival, growth, tumorigenesis, and metabolism. TAK1 signaling also upregulates AMPK activity and autophagy. Here, we investigated T...
  19. Toll-like receptor 7-mediated type I interferon signaling prevents cholestasis- and hepatotoxin-induced liver fibrosis.

    Hepatology 60(1):237 (2014) PMID 24375615

    Toll-like receptor 7 (TLR7) signaling predominantly regulates production of type I interferons (IFNs), which has been suggested in clinical studies to be antifibrotic. However, the mechanistic role of the TLR7-type I IFN axis in liver fibrosis has not been elucidated. In the present study, liver...
  20. Liver damage, inflammation, and enhanced tumorigenesis after persistent mTORC1 inhibition.

    Cell Metabolism 20(1):133 (2014) PMID 24910242 PMCID PMC4079758

    Obesity can result in insulin resistance, hepatosteatosis, and nonalcoholic steatohepatitis (NASH) and increases liver cancer risk. Obesity-induced insulin resistance depends, in part, on chronic activation of mammalian target of rapamycin complex 1 (mTORC1), which also occurs in human and mouse...