1. 24-nor-ursodeoxycholic acid ameliorates inflammatory response and liver fibrosis in a murine model of hepatic schistosomiasis

    Journal of Hepatology 62(4):871 (2015)

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  2. Adenoma-linked barrier defects and microbial products drive IL-23/IL-17-mediated tumour growth.

    Nature 491(7423):254 (2012) PMID 23034650 PMCID PMC3601659

    Approximately 2% of colorectal cancer is linked to pre-existing inflammation known as colitis-associated cancer, but most develops in patients without underlying inflammatory bowel disease. Colorectal cancer often follows a genetic pathway whereby loss of the adenomatous polyposis coli (APC) tum...
  3. Adenoma-linked barrier defects and microbial products drive IL-23/IL-17-mediated tumour growth.

    Nature 491(7423):254 (2012) PMID 23034650 PMCID PMC3601659

    Approximately 2% of colorectal cancer is linked to pre-existing inflammation known as colitis-associated cancer, but most develops in patients without underlying inflammatory bowel disease. Colorectal cancer often follows a genetic pathway whereby loss of the adenomatous polyposis coli (APC) tum...
  4. Interleukin-17 signaling in inflammatory, Kupffer cells, and hepatic stellate cells exacerbates liver fibrosis in mice.

    Gastroenterology 143(3):765 (2012) PMID 22687286 PMCID PMC3635475

    Interleukin (IL)-17 signaling has been implicated in lung and skin fibrosis. We examined the role of IL-17 signaling in the pathogenesis of liver fibrosis in mice. Using cholestatic and hepatotoxic models of liver injury, we compared the development of liver fibrosis in wild-type mice with that ...
  5. Interleukin-17 Signaling in Inflammatory, Kupffer Cells, and Hepatic Stellate Cells Exacerbates Liver Fibrosis in Mice

    Gastroenterology 143(3):765 (2012)

    Background & Aims Interleukin (IL)-17 signaling has been implicated in lung and skin fibrosis. We examined the role of IL-17 signaling in the pathogenesis of liver fibrosis in mice.
  6. Xenobiotic-induced liver injury and fibrosis.

    Expert Opinion on Drug Metabolism and Toxicology 8(5):571 (2012) PMID 22452290

    Many different drugs and xenobiotics (chemical compounds foreign to an organism) can injure the bile duct epithelium and cause inflammatory bile duct diseases (cholangiopathies) ranging from transient cholestasis to vanishing bile duct syndrome, sclerosing cholangitis with development of biliary...
  7. Animal models of biliary tract injury.

    Current Opinion in Gastroenterology 28(3):239 (2012) PMID 22450892

    Cholestatic liver diseases with bile duct injury and biliary fibrosis account for a significant percentage of patients with end-stage liver disease and undergoing liver transplantation. A number of different animal models have been established and have added substantially to our understanding of...
  8. The nicotinamide adenine dinucleotide phosphate oxidase (NOX) homologues NOX1 and NOX2/gp91(phox) mediate hepatic fibrosis in mice.

    Hepatology 53(5):1730 (2011) PMID 21384410 PMCID PMC3082608

    Nicotinamide adenine dinucleotide phosphate oxidase (NOX) is a multicomponent enzyme that mediates electron transfer from nicotinamide adenine dinucleotide phosphate to molecular oxygen, which leads to the production of superoxide. NOX2/gp91(phox) is a catalytic subunit of NOX expressed in phago...
  9. Fibrosis in Autoimmune and Cholestatic Liver Disease

    Best Practice & Research Clinical Gastroenterology 25(2):245 (2011)

    Autoimmune and cholestatic liver disease account for a significant part of end-stage liver disease and are leading indications for liver transplantation. Especially cholestatic liver diseases (primary biliary cirrhosis and primary sclerosing cholangitis) appear to be different from oth...
  10. Fibrosis in autoimmune and cholestatic liver disease.

    Best Practice & Research Clinical Gastroenterology 25(2):245 (2011) PMID 21497742 PMCID PMC3134112

    Autoimmune and cholestatic liver disease account for a significant part of end-stage liver disease and are leading indications for liver transplantation. Especially cholestatic liver diseases (primary biliary cirrhosis and primary sclerosing cholangitis) appear to be different from other chronic...
  11. Fibroblast-specific protein 1 identifies an inflammatory subpopulation of macrophages in the liver.

    PNAS 108(1):308 (2011) PMID 21173249 PMCID PMC3017162

    Cirrhosis is the end result of chronic liver disease. Hepatic stellate cells (HSC) are believed to be the major source of collagen-producing myofibroblasts in cirrhotic livers. Portal fibroblasts, bone marrow-derived cells, and epithelial to mesenchymal transition (EMT) might also contribute to ...
  12. JAK-STAT signaling in hepatic fibrosis.

    Frontiers in Bioscience 16:2794 (2011) PMID 21622209

    Chronic liver injury, liver fibrosis and formation of hepatocellular carcinoma are intimately linked and represent a major medical challenge since treatment options are limited. Therefore, it is important to identify cellular and molecular pathways that promote liver damage or provide hepatoprot...
  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. Genetic labeling does not detect epithelial-to-mesenchymal transition of cholangiocytes in liver fibrosis in mice.

    Gastroenterology 139(3):987 (2010) PMID 20546735 PMCID PMC2930026

    Chronic injury changes the fate of certain cellular populations, inducing epithelial cells to generate fibroblasts by epithelial-to-mesenchymal transition (EMT) and mesenchymal cells to generate epithelial cells by mesenchymal-to-epithelial transition (MET). Although contribution of EMT/MET to e...
  15. Hepatocytes do not undergo epithelial-mesenchymal transition in liver fibrosis in mice.

    Hepatology 51(3):1027 (2010) PMID 20052656 PMCID PMC2906231

    The origin of fibrogenic cells in liver fibrosis remains controversial. We assessed the emerging concept that hepatocytes contribute to production of extracellular matrix (ECM) in liver fibrosis through epithelial-mesenchymal transition (EMT). We bred triple transgenic mice expressing ROSA26 sto...
  16. Dietary and Genetic Obesity Promote Liver Inflammation and Tumorigenesis by Enhancing IL-6 and TNF Expression

    Cell 140(2):197 (2010)

    Epidemiological studies indicate that overweight and obesity are associated with increased cancer risk. To study how obesity augments cancer risk and development, we focused on hepatocellular carcinoma (HCC), the common form of liver cancer whose occurrence and progression are the most...
  17. Dietary and genetic obesity promote liver inflammation and tumorigenesis by enhancing IL-6 and TNF expression.

    Cell 140(2):197 (2010) PMID 20141834 PMCID PMC2836922

    Epidemiological studies indicate that overweight and obesity are associated with increased cancer risk. To study how obesity augments cancer risk and development, we focused on hepatocellular carcinoma (HCC), the common form of liver cancer whose occurrence and progression are the most strongly ...
  18. Disruption of TAK1 in hepatocytes causes hepatic injury, inflammation, fibrosis, and carcinogenesis.

    PNAS 107(2):844 (2010) PMID 20080763 PMCID PMC2818947

    TGF-beta-activated kinase 1 (TAK1) is a MAP3K family member that activates NF-kappaB and JNK via Toll-like receptors and the receptors for IL-1, TNF-alpha, and TGF-beta. Because the TAK1 downstream molecules NF-kappaB and JNK have opposite effects on cell death and carcinogenesis, the role of TA...
  19. Genetic Labeling Does Not Detect Epithelial-to-Mesenchymal Transition of Cholangiocytes in Liver Fibrosis in Mice

    Gastroenterology 139(3):987 (2010)

    Background & Aims Chronic injury changes the fate of certain cellular populations, inducing epithelial cells to generate fibroblasts by epithelial-to-mesenchymal transition (EMT) and mesenchymal cells to generate epithelial cells by mesenchymal-to-epithelial transition (MET). Although ...
  20. 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.