1. Arginine and NASH--do macrophages deliver the first hit?

    Journal of Hepatology 62(2):260 (2015) PMID 25450197

  2. Arginine and NASH - Do macrophages deliver the first hit?

    Journal of Hepatology 62(2):260 (2015) PMID 25450197

  3. Arginine and NASH--do macrophages deliver the first hit?

    Journal of Hepatology 62(2):260 (2015) PMID 25450197

  4. Genetic dissection of retinoid esterification and accumulation in the liver and adipose tissue.

    Journal of Lipid Research 55(1):104 (2014) PMID 24186946 PMCID PMC3927479

    Approximately 80-90% of all retinoids in the body are stored as retinyl esters (REs) in the liver. Adipose tissue also contributes significantly to RE storage. The present studies, employing genetic and nutritional interventions, explored factors that are responsible for regulating RE accumulati...
  5. Genetic dissection of retinoid esterification and accumulation in the liver and adipose tissue.

    Journal of Lipid Research 55(1):104 (2014) PMID 24186946 PMCID PMC3927479

    Approximately 80-90% of all retinoids in the body are stored as retinyl esters (REs) in the liver. Adipose tissue also contributes significantly to RE storage. The present studies, employing genetic and nutritional interventions, explored factors that are responsible for regulating RE accumulati...
  6. Hepatic macrophages but not dendritic cells contribute to liver fibrosis by promoting the survival of activated hepatic stellate cells in mice.

    Hepatology 58(4):1461 (2013) PMID 23553591 PMCID PMC3848418

    Although it is well established that hepatic macrophages play a crucial role in the development of liver fibrosis, the underlying mechanisms remain largely elusive. Moreover, it is not known whether other mononuclear phagocytes such as dendritic cells (DCs) contribute to hepatic stellate cell (H...
  7. Hepatic macrophages but not dendritic cells contribute to liver fibrosis by promoting the survival of activated hepatic stellate cells in mice.

    Hepatology 58(4):1461 (2013) PMID 23553591 PMCID PMC3848418

    Although it is well established that hepatic macrophages play a crucial role in the development of liver fibrosis, the underlying mechanisms remain largely elusive. Moreover, it is not known whether other mononuclear phagocytes such as dendritic cells (DCs) contribute to hepatic stellate cell (H...
  8. Induction of heme oxygenase 1 prevents progression of liver fibrosis in Mdr2 knockout mice.

    Hepatology 55(2):553 (2012) PMID 21953613

    Induction or overexpression of the heme-degrading enzyme, heme oxygenase 1 (HO-1), has been shown to protect mice from liver damage induced by acute inflammation. We have investigated the effects of HO-1 induction in a mouse model of chronic liver inflammation and fibrogenesis with progression t...
  9. Induction of heme oxygenase 1 prevents progression of liver fibrosis in Mdr2 knockout mice.

    Hepatology 55(2):553 (2012) PMID 21953613

    Induction or overexpression of the heme-degrading enzyme, heme oxygenase 1 (HO-1), has been shown to protect mice from liver damage induced by acute inflammation. We have investigated the effects of HO-1 induction in a mouse model of chronic liver inflammation and fibrogenesis with progression t...
  10. Absence of hepatic stellate cell retinoid lipid droplets does not enhance hepatic fibrosis but decreases hepatic carcinogenesis.

    Gut 60(9):1260 (2011) PMID 21278145

    Hepatic stellate cells (HSCs) contain a number of bioactive metabolites or their precursors including retinoids in their characteristic lipid droplets. The loss of lipid droplets and retinoids is a hallmark of HSC activation, but it remains unclear whether this loss promotes HSC activation, live...
  11. Absence of hepatic stellate cell retinoid lipid droplets does not enhance hepatic fibrosis but decreases hepatic carcinogenesis.

    Gut 60(9):1260 (2011) PMID 21278145

    Hepatic stellate cells (HSCs) contain a number of bioactive metabolites or their precursors including retinoids in their characteristic lipid droplets. The loss of lipid droplets and retinoids is a hallmark of HSC activation, but it remains unclear whether this loss promotes HSC activation, live...
  12. Role and cellular source of nicotinamide adenine dinucleotide phosphate oxidase in hepatic fibrosis.

    Hepatology 52(4):1420 (2010) PMID 20690191 PMCID PMC2947612

    Reactive oxygen species (ROS) generated by nicotinamide adenine dinucleotide phosphate oxidase (NOX) is required for liver fibrosis. This study investigates the role of NOX in ROS production and the differential contribution of NOX from bone marrow (BM)-derived and non-BM-derived liver cells. He...
  13. Role and cellular source of nicotinamide adenine dinucleotide phosphate oxidase in hepatic fibrosis.

    Hepatology 52(4):1420 (2010) PMID 20690191 PMCID PMC2947612

    Reactive oxygen species (ROS) generated by nicotinamide adenine dinucleotide phosphate oxidase (NOX) is required for liver fibrosis. This study investigates the role of NOX in ROS production and the differential contribution of NOX from bone marrow (BM)-derived and non-BM-derived liver cells. He...
  14. Modulation of Hepatic Fibrosis by c-Jun-N-Terminal Kinase Inhibition

    Gastroenterology 138(1):347 (2010) PMID 19782079 PMCID PMC2988578

    Background & Aims c-Jun N-terminal kinase (JNK) is activated by multiple profibrogenic mediators; JNK activation occurs during toxic, metabolic, and autoimmune liver injury. However, its role in hepatic fibrogenesis is unknown.
  15. Modulation of Hepatic Fibrosis by c-Jun-N-Terminal Kinase Inhibition

    Gastroenterology 138(1):347 (2010)

    Background & Aims c-Jun N-terminal kinase (JNK) is activated by multiple profibrogenic mediators; JNK activation occurs during toxic, metabolic, and autoimmune liver injury. However, its role in hepatic fibrogenesis is unknown.
  16. Modulation of hepatic fibrosis by c-Jun-N-terminal kinase inhibition.

    Gastroenterology 138(1):347 (2010) PMID 19782079 PMCID PMC2988578

    c-Jun N-terminal kinase (JNK) is activated by multiple profibrogenic mediators; JNK activation occurs during toxic, metabolic, and autoimmune liver injury. However, its role in hepatic fibrogenesis is unknown. JNK phosphorylation was detected by immunoblot analysis and confocal immunofluorescent...
  17. Modulation of Hepatic Fibrosis by c-Jun-N-Terminal Kinase Inhibition

    Gastroenterology 138(1):347 (2010) PMID 19782079 PMCID PMC2988578

    Background & Aims c-Jun N-terminal kinase (JNK) is activated by multiple profibrogenic mediators; JNK activation occurs during toxic, metabolic, and autoimmune liver injury. However, its role in hepatic fibrogenesis is unknown.
  18. Angiotensin-converting-enzyme 2 inhibits liver fibrosis in mice.

    Hepatology 50(3):929 (2009) PMID 19650157

    The renin-angiotensin system (RAS) plays a major role in liver fibrosis. Recently, a homolog of angiotensin-converting-enzyme 1 (ACE1), termed ACE2, has been identified that appears to be a negative regulator of the RAS by degrading Ang II to Ang(1-7). The aim of this study was to characterize t...
  19. Angiotensin-converting-enzyme 2 inhibits liver fibrosis in mice.

    Hepatology 50(3):929 (2009) PMID 19650157

    The renin-angiotensin system (RAS) plays a major role in liver fibrosis. Recently, a homolog of angiotensin-converting-enzyme 1 (ACE1), termed ACE2, has been identified that appears to be a negative regulator of the RAS by degrading Ang II to Ang(1-7). The aim of this study was to characterize t...
  20. CCR1 and CCR5 promote hepatic fibrosis in mice.

    Journal of Clinical Investigation 119(7):1858 (2009) PMID 19603542 PMCID PMC2701864

    Hepatic fibrosis develops as a response to chronic liver injury and almost exclusively occurs in a proinflammatory environment. However, the role of inflammatory mediators in fibrogenic responses of the liver is only poorly understood. We therefore investigated the role of CC chemokines and thei...