Biography
Clinically, metabolic dysfunction associated steatohepatitis (MASH) is becoming the leading cause of chronic liver disease and liver cancer, and her lab is interested in deciphering how dynamic changes in the liver matrix accelerate this process in certain conditions such as type 2 diabetes. Of particular interest are studies on collagen architecture and connectivity and how these are implicated in mechano-sensing. They also explore aging-related pathways in wound healing processes, and how these intersect with innate immune responses and matrix modulation in the liver. Based on these studies they are identifying targets to treat fibrosis, and are performing investigator-initiated clinical trials. As fatty liver is becoming the most common liver disease in the US and worldwide the ultimate goal is to target high-risk populations, and to develop novel surveillance and therapeutic approaches.
Professional Summary
Education & Certifications
- Board Certification: American Board of Internal Medicine, Gastroenterology (2003)
- Residency: Mayo Clinic Internal Medicine Residency (1999) MN
- Board Certification, American Board of Internal Medicine, Gastroenterology (2004)
-
- Fellowship: Mayo Clinic Gastroenterology Fellowship (2003) MN
- Medical Education: Semmelweis Univ Med School (1988) Hungary
Honors & Awards
- Boris Ruebner and John Rosenquist Excellence in Teaching Award, UC Davis (2014)
- elected member, American Society for Clinical Investigation (2014)
- Fellow, American Association for Studies of Liver Diseases (2016)
-
Memberships
- Associate Editor, Hepatology (2021 - Present)
- Associate Editor, Seminars in Liver Disease (2017 - Present)
- Associate Editor, Hepatology Communications (2017 - 2021)
-
- Associate Editor, American Journal of Physiology Gastrointestinal and Liver Physiology (2015 - 2018)
- Data Monitoring Committee, NASH Clinical Research Network, NIH (2012 - Present)
- Regular member, NIH HBPP Study Section (2012 - 2016)
Administrative Appointments
- Department of Medicine Team Science Division Representative, Department of Medicine (2023 - Present)
- Director of the T32 Program, Division of Gastroenterology and Hepatology (2019 - Present)
- Vice Chief of Research, Division of Gastroenterology and Hepatology (2020 - Present)
-
Publications
-
Neutrophil-Hepatic Stellate Cell Interactions Promote Fibrosis in Experimental Steatohepatitis.
Zhou, Z., Xu, M.-J. J., Cai, Y., Wang, W., Jiang, J. X., Varga, Z. V., … Gao, B. (2018). Neutrophil-Hepatic Stellate Cell Interactions Promote Fibrosis in Experimental Steatohepatitis. Cellular and Molecular Gastroenterology and Hepatology, 5(3), 399–413. -
The NOX1 isoform of NADPH oxidase is involved in dysfunction of liver sinusoids in nonalcoholic fatty liver disease.
Matsumoto, M., Zhang, J., Zhang, X., Liu, J., Jiang, J. X., Yamaguchi, K., … Yabe-Nishimura, C. (2018). The NOX1 isoform of NADPH oxidase is involved in dysfunction of liver sinusoids in nonalcoholic fatty liver disease. Free Radical Biology & Medicine, 115, 412–20. -
TRIF as a Novel Modulator of Liver Inflammation and Fibrosis.
Török, N. J. (2017). TRIF as a Novel Modulator of Liver Inflammation and Fibrosis. Cellular and Molecular Gastroenterology and Hepatology, 3(3), 299–300. -
-
Ductular reaction-on-a-chip: Microfluidic co-cultures to study stem cell fate selection during liver injury
Haque, A., Gheibi, P., Stybayeva, G., Gao, Y., Torok, N., & Revzin, A. (2016). Ductular reaction-on-a-chip: Microfluidic co-cultures to study stem cell fate selection during liver injury. SCIENTIFIC REPORTS, 6. -
Metabolic Syndrome Post-Liver Transplant: Can We Predict?
Marsano, J. G., & Torok, N. J. (2016). Metabolic Syndrome Post-Liver Transplant: Can We Predict? METABOLIC SYNDROME AND RELATED DISORDERS, 14(6), 289–90. -
Dysregulation of redox pathways in liver fibrosis
Torok, N. J. (2016). Dysregulation of redox pathways in liver fibrosis. AMERICAN JOURNAL OF PHYSIOLOGY-GASTROINTESTINAL AND LIVER PHYSIOLOGY, 311(4), G667–G674. -
Vascular adhesion protein 1 in nonalcoholic steatohepatitis: A novel biomarker?
Torok, N. J. (2015). Vascular adhesion protein 1 in nonalcoholic steatohepatitis: A novel biomarker? HEPATOLOGY, 62(4), 1313–15. -
Galectin-3 regulates inflammasome activation in cholestatic liver injury
Tian, J., Yang, G., Chen, H.-Y., Hsu, D. K., Tomilov, A., Olson, K. A., … Jiang, J. X. (2016). Galectin-3 regulates inflammasome activation in cholestatic liver injury. FASEB JOURNAL, 30(12), 4202–13. -
Extracellular vesicles and ceramide: new mediators for macrophage chemotaxis?
Toeroek, N. J. (2016). Extracellular vesicles and ceramide: new mediators for macrophage chemotaxis? JOURNAL OF LIPID RESEARCH, 57(2), 157–58. -
Galectin 3 regulates HCC cell invasion by RhoA and MLCK activation
Serizawa, N., Tian, J., Fukada, H., Baghy, K., Scott, F., Chen, X., … Jiang, J. X. (2015). Galectin 3 regulates HCC cell invasion by RhoA and MLCK activation. LABORATORY INVESTIGATION, 95(10), 1145–56. -
Calciphylaxis in a Patient With Alcoholic Cirrhosis.
Akhtar, E., Parikh, D. A., & Torok, N. J. (2015). Calciphylaxis in a Patient With Alcoholic Cirrhosis. ACG Case Reports Journal, 2(4), 209–10. -
Hepatocyte Nicotinamide Adenine Dinucleotide Phosphate Reduced Oxidase 4 Regulates Stress Signaling, Fibrosis, and Insulin Sensitivity During Development of Steatohepatitis in Mice
Bettaieb, A., Jiang, J. X., Sasaki, Y., Chao, T.-I., Kiss, Z., Chen, X., … Toeroek, N. J. (2015). Hepatocyte Nicotinamide Adenine Dinucleotide Phosphate Reduced Oxidase 4 Regulates Stress Signaling, Fibrosis, and Insulin Sensitivity During Development of Steatohepatitis in Mice. GASTROENTEROLOGY, 149(2), 468-? -
Update on Alcoholic Hepatitis.
Torok, N. J. (2015). Update on Alcoholic Hepatitis. Biomolecules, 5(4), 2978–86. -
Role of intestinal myofibroblasts in HIV-associated intestinal collagen deposition and immune reconstitution following combination antiretroviral therapy
Asmuth, D. M., Pinchuk, I. V., Wu, J., Vargas, G., Chen, X., Mann, S., … Powell, D. W. (2015). Role of intestinal myofibroblasts in HIV-associated intestinal collagen deposition and immune reconstitution following combination antiretroviral therapy. AIDS, 29(8), 877–88. -
Strategies and endpoints of antifibrotic drug trials: Summary and recommendations from the AASLD Emerging Trends Conference, Chicago, June 2014
Torok, N. J., Dranoff, J. A., Schuppan, D., & Friedman, S. L. (2015). Strategies and endpoints of antifibrotic drug trials: Summary and recommendations from the AASLD Emerging Trends Conference, Chicago, June 2014. HEPATOLOGY, 62(2), 627–34. -
MLK3 as a regulator of disease progression in Non-alcoholic steatohepatitis
Jiang, J. X., & Toeroek, N. J. (2014). MLK3 as a regulator of disease progression in Non-alcoholic steatohepatitis. LIVER INTERNATIONAL, 34(8), 1131–32. -
Liver Injury and the Activation of the Hepatic Myofibroblasts.
Jiang, J. X., & Török, N. J. (2013). Liver Injury and the Activation of the Hepatic Myofibroblasts. Current Pathobiology Reports, 1(3), 215–23. -
Role of FNA and Core Biopsy of Primary and Metastatic Liver Disease.
McGahan, J. P., Bishop, J., Webb, J., Howell, L., Torok, N., Lamba, R., & Corwin, M. T. (2013). Role of FNA and Core Biopsy of Primary and Metastatic Liver Disease. International Journal of Hepatology, 2013, 174103-? -
Advanced glycation endproducts induce fibrogenic activity in nonalcoholic steatohepatitis by modulating TNF-a-converting enzyme activity in mice.
Jiang, J. X., Chen, X., Fukada, H., Serizawa, N., Devaraj, S., & Török, N. J. (2013). Advanced glycation endproducts induce fibrogenic activity in nonalcoholic steatohepatitis by modulating TNF-a-converting enzyme activity in mice. Hepatology , 58(4), 1339–48. -
Wilson's Disease: Changes in Methionine Metabolism and Inflammation Affect Global DNA Methylation in Early Liver Disease
Medici, V., Shibata, N. M., Kharbanda, K. K., LaSalle, J. M., Woods, R., Liu, S., … Halsted, C. H. (2013). Wilson's Disease: Changes in Methionine Metabolism and Inflammation Affect Global DNA Methylation in Early Liver Disease. HEPATOLOGY, 57(2), 555–65. -
Human ESC self-renewal promoting microRNAs induce epithelial-mesenchymal transition in hepatocytes by controlling the PTEN and TGFß tumor suppressor signaling pathways.
Jung, C. J., Iyengar, S., Blahnik, K. R., Jiang, J. X., Tahimic, C., Torok, N. J., … Zern, M. (2012). Human ESC self-renewal promoting microRNAs induce epithelial-mesenchymal transition in hepatocytes by controlling the PTEN and TGFß tumor suppressor signaling pathways. Molecular Cancer Research , 10(7), 979–91. -
Liver fibrosis and hepatocyte apoptosis are attenuated by GKT137831, a novel NOX4/NOX1 inhibitor in vivo
Jiang, J. X., Chen, X., Serizawa, N., Szyndralewiez, C., Page, P., Schroeder, K., … Toeroek, N. J. (2012). Liver fibrosis and hepatocyte apoptosis are attenuated by GKT137831, a novel NOX4/NOX1 inhibitor in vivo. FREE RADICAL BIOLOGY AND MEDICINE, 53(2), 289–96. -
Galectin-3 modulates phagocytosis-induced stellate cell activation and liver fibrosis in vivo
Jiang, J. X., Chen, X., Hsu, D. K., Baghy, K., Serizawa, N., Scott, F., … Toeroek, N. J. (2012). Galectin-3 modulates phagocytosis-induced stellate cell activation and liver fibrosis in vivo. AMERICAN JOURNAL OF PHYSIOLOGY-GASTROINTESTINAL AND LIVER PHYSIOLOGY, 302(4), G439–G446. -
Leptin: The missing link between obesity and heart disease?
Devaraj, S., & Torok, N. (2011). Leptin: The missing link between obesity and heart disease? ATHEROSCLEROSIS, 217(2), 322–23. -
NOX1/Nicotinamide Adenine Dinucleotide Phosphate, Reduced Form (NADPH) Oxidase Promotes Proliferation of Stellate Cells and Aggravates Liver Fibrosis Induced by Bile Duct Ligation
Cui, W., Matsuno, K., Iwata, K., Ibi, M., Matsumoto, M., Zhang, J., … Yabe-Nishimura, C. (2011). NOX1/Nicotinamide Adenine Dinucleotide Phosphate, Reduced Form (NADPH) Oxidase Promotes Proliferation of Stellate Cells and Aggravates Liver Fibrosis Induced by Bile Duct Ligation. HEPATOLOGY, 54(3), 949–58. -
Molecular Characterization of Stool Microbiota in HIV-Infected Subjects by Panbacterial and Order-Level 16S Ribosomal DNA (rDNA) Quantification and Correlations With Immune Activation
Ellis, C. L., Ma, Z.-M., Mann, S. K., Li, C.-S., Wu, J., Knight, T. H., … Asmuth, D. M. (2011). Molecular Characterization of Stool Microbiota in HIV-Infected Subjects by Panbacterial and Order-Level 16S Ribosomal DNA (rDNA) Quantification and Correlations With Immune Activation. JAIDS-JOURNAL OF ACQUIRED IMMUNE DEFICIENCY SYNDROMES, 57(5), 363–70. -
Genomic variants associated with primary biliary cirrhosis.
Selmi, C., Torok, N. J., Affronti, A., & Gershwin, M. E. (2010). Genomic variants associated with primary biliary cirrhosis. Genome Medicine, 2(1), 5-? -
Reduced Nicotinamide Adenine Dinucleotide Phosphate Oxidase 2 Plays a Key Role in Stellate Cell Activation and Liver Fibrogenesis In Vivo
Jiang, J. X., Venugopal, S., Serizawa, N., Chen, X., Scott, F., Li, Y., … Toeroek, N. J. (2010). Reduced Nicotinamide Adenine Dinucleotide Phosphate Oxidase 2 Plays a Key Role in Stellate Cell Activation and Liver Fibrogenesis In Vivo. GASTROENTEROLOGY, 139(4), 1375-? -
Increased Soluble Leptin Receptor Levels in Morbidly Obese Patients With Insulin Resistance and Nonalcoholic Fatty Liver Disease
Medici, V., Ali, M. R., Seo, S., Aoki, C. A., Rossaro, L., Kim, K., … Toeroek, N. J. (2010). Increased Soluble Leptin Receptor Levels in Morbidly Obese Patients With Insulin Resistance and Nonalcoholic Fatty Liver Disease. OBESITY, 18(12), 2268–73. -
Liver fibrosis causes downregulation of miRNA-150 and miRNA-194 in hepatic stellate cells, and their overexpression causes decreased stellate cell activation
Venugopal, S. K., Jiang, J., Kim, T.-H., Li, Y., Wang, S.-S., Torok, N. J., … Zern, M. A. (2010). Liver fibrosis causes downregulation of miRNA-150 and miRNA-194 in hepatic stellate cells, and their overexpression causes decreased stellate cell activation. AMERICAN JOURNAL OF PHYSIOLOGY-GASTROINTESTINAL AND LIVER PHYSIOLOGY, 298(1), G101–G106. -
Apoptotic body engulfment by hepatic stellate cells promotes their survival by the JAK/STAT and Akt/NF-kappaB-dependent pathways.
Jiang, J. X., Mikami, K., Venugopal, S., Li, Y., & Torok, N. J. (2009). Apoptotic body engulfment by hepatic stellate cells promotes their survival by the JAK/STAT and Akt/NF-kappaB-dependent pathways. JOURNAL OF HEPATOLOGY, 51(1), 139–48. -
Retinitis pigmentosa with special reference to otologic, neurologic, and endocrine complications.
KJERRUMGAARD, E. (1948). Retinitis pigmentosa with special reference to otologic, neurologic, and endocrine complications. Acta Ophthalmologica, 26(1), 55–65. -
Keratin 19 as a biochemical marker of skin stem cells in vivo and in vitro: Keratin 19 expressing cells are differentially localized in function of anatomic sites, and their number varies with donor age and culture stage
Michel, M., Torok, N., Godbout, M. J., Lussier, M., GAUDREAU, P., Royal, A., & GERMAIN, L. (1996). Keratin 19 as a biochemical marker of skin stem cells in vivo and in vitro: Keratin 19 expressing cells are differentially localized in function of anatomic sites, and their number varies with donor age and culture stage. JOURNAL OF CELL SCIENCE, 109, 1017–28. -
Upregulation of molecular motor-encoding genes during hepatocyte growth factor- and epidermal growth factor-induced cell motility
Torok, N., Urrutia, R., Nakamura, T., & McNiven, M. A. (1996). Upregulation of molecular motor-encoding genes during hepatocyte growth factor- and epidermal growth factor-induced cell motility. JOURNAL OF CELLULAR PHYSIOLOGY, 167(3), 422–33. -
Vesicle movement in rat hepatocytes is reduced by ethanol exposure: Alterations in microtubule-based motor enzymes
Torok, N., Marks, D., Hsiao, K., Oswald, B. J., & McNiven, M. A. (1997). Vesicle movement in rat hepatocytes is reduced by ethanol exposure: Alterations in microtubule-based motor enzymes. GASTROENTEROLOGY, 113(6), 1938–48. -
Alterations in vesicle transport and cell polarity in rat hepatocytes subjected to mechanical or chemical cholestasis
Torok, N. J., Larusso, E. M., & McNiven, M. A. (2001). Alterations in vesicle transport and cell polarity in rat hepatocytes subjected to mechanical or chemical cholestasis. GASTROENTEROLOGY, 121(5), 1176–84. -
Cholangiocarcinoma.
Torok, N., & Gores, G. J. (2001). Cholangiocarcinoma. Seminars in Gastrointestinal Disease, 12(2), 125–32. -
Nitric oxide inhibits apoptosis downstream of cytochrome c release by nitrosylating caspase 9
Torok, N. J., Higuchi, H., Bronk, S., & Gores, G. J. (2002). Nitric oxide inhibits apoptosis downstream of cytochrome c release by nitrosylating caspase 9. CANCER RESEARCH, 62(6), 1648–53. -
Apoptotic body engulfment by a human stellate cell line is profibrogenic
Canbay, A., Taimr, P., Torok, N., Higuchi, H., Friedman, S., & Gores, G. J. (2003). Apoptotic body engulfment by a human stellate cell line is profibrogenic. LABORATORY INVESTIGATION, 83(5), 655–63. -
Phagocytosis of apoptotic bodies by hepatic stellate cells induces NADPH oxidase and is associated with liver fibrosis in vivo
Zhan, S. S., jiang, J. X., Wu, J., Halsted, C., Friedman, S. L., Zern, M. A., & Torok, N. J. (2006). Phagocytosis of apoptotic bodies by hepatic stellate cells induces NADPH oxidase and is associated with liver fibrosis in vivo. HEPATOLOGY, 43(3), 435–43. -
Apoptotic cell death takes its toll
Torok, N. J. (2007). Apoptotic cell death takes its toll. HEPATOLOGY, 46(5), 1323–25. -
Nonalcoholic steatohepatitis and the metabolic syndrome.
Jiang, J., & Torok, N. (2008). Nonalcoholic steatohepatitis and the metabolic syndrome. Metabolic Syndrome and Related Disorders, 6(1), 1–7. -
Minocycline in the Treatment of Patients With Primary Sclerosing Cholangitis: Results of a Pilot Study
Silveira, M. G., Torok, N. J., Gossard, A. A., Keach, J. C., Jorgensen, R. A., Petz, J. L., & Lindor, K. D. (2009). Minocycline in the Treatment of Patients With Primary Sclerosing Cholangitis: Results of a Pilot Study. AMERICAN JOURNAL OF GASTROENTEROLOGY, 104(1), 83–88. -
Adenosine Induces Loss of Actin Stress Fibers and Inhibits Contraction in Hepatic Stellate Cells via Rho Inhibition
Sohail, M. A., Hashmi, A. Z., Hakim, W., Watanabe, A., Zipprich, A., Groszmann, R. J., … Mehal, W. Z. (2009). Adenosine Induces Loss of Actin Stress Fibers and Inhibits Contraction in Hepatic Stellate Cells via Rho Inhibition. HEPATOLOGY, 49(1), 185–94. -
Digoxin Suppresses Pyruvate Kinase M2-Promoted HIF-1a Transactivation in Steatohepatitis.
Ouyang, X., Han, S.-N. N., Zhang, J.-Y. Y., Dioletis, E., Nemeth, B. T., Pacher, P., … Mehal, W. Z. (2018). Digoxin Suppresses Pyruvate Kinase M2-Promoted HIF-1a Transactivation in Steatohepatitis. Cell Metabolism, 27(5), 1156. -
P300, A New Player in Mechanosensitivity and Activation of Cancer-Associated Fibroblasts.
Torok, N. J. (2018). P300, A New Player in Mechanosensitivity and Activation of Cancer-Associated Fibroblasts. Gastroenterology, 154(8), 2025–2026. -
Leptin Induces Phagocytosis of Apoptotic Bodies by Hepatic Stellate Cells via a Rho Guanosine Triphosphatase-Dependent Mechanism
Jiang, J. X., Mikami, K., Shah, V. H., & Torok, N. J. (2008). Leptin Induces Phagocytosis of Apoptotic Bodies by Hepatic Stellate Cells via a Rho Guanosine Triphosphatase-Dependent Mechanism. HEPATOLOGY, 48(5), 1497–1505. -
Recent advances in the pathogenesis and diagnosis of liver fibrosis
Torok, N. J. (2008). Recent advances in the pathogenesis and diagnosis of liver fibrosis. JOURNAL OF GASTROENTEROLOGY, 43(5), 315–21. -
Adiponectin decreases C-reactive protein synthesis and secretion from endothelial cells - Evidence for an adipose tissue-vascular loop
Devaraj, S., Torok, N., Dasu, M. R., Samols, D., & Jialal, I. (2008). Adiponectin decreases C-reactive protein synthesis and secretion from endothelial cells - Evidence for an adipose tissue-vascular loop. ARTERIOSCLEROSIS THROMBOSIS AND VASCULAR BIOLOGY, 28(7), 1368–74. -
AGER1/RAGE imbalance and accumulation of AGEs result in inflammation, expansion of ductular cells and fibrosis in NASH
Dehnad, A., Wong, K. A., Fish, S., Jiang, J., Alzofon, N., Olson, K., … Torok, N. J. (2017). AGER1/RAGE imbalance and accumulation of AGEs result in inflammation, expansion of ductular cells and fibrosis in NASH. HEPATOLOGY, 66, 210A. -
Activation of NOX2 in older mice by the aging protein p52Shc leads to accelerated fibrosis in NASH
Fish, S., Tomilov, A., Dehnad, A., Jiang, J., Alzofon, N., Das, S., … Torok, N. J. (2017). Activation of NOX2 in older mice by the aging protein p52Shc leads to accelerated fibrosis in NASH. HEPATOLOGY, 66, 208A. -
Advanced glycation end products and dysregulated RAGE/AGER1 induce proinflammatory and fibrogenic signaling in NASH via NOX4
Dehnad, A., Fish, S., Jiang, J., & Torok, N. J. (2016). Advanced glycation end products and dysregulated RAGE/AGER1 induce proinflammatory and fibrogenic signaling in NASH via NOX4. HEPATOLOGY, 64, 830A. -
Aged mice exhibit a more proinflammatory and fibrogenic NASH phenotype linked to the induction of Shc and NADPH oxidase 2
Fish, S., Dehnad, A., Jiang, J., Tomilov, A., Ramsey, J., Cortopassi, G., & Torok, N. J. (2016). Aged mice exhibit a more proinflammatory and fibrogenic NASH phenotype linked to the induction of Shc and NADPH oxidase 2. HEPATOLOGY, 64, 825A. -
Hepatocyte NOX4 plays an important role in modulating stress response-mediated fibrogenic injury during NASH
chao, T.-I., Jiang, X., Fukada, H., Haj, F., Bettaieb, A., & Torok, N. (2013). Hepatocyte NOX4 plays an important role in modulating stress response-mediated fibrogenic injury during NASH. HEPATOLOGY, 58, 221A. -
Calciphylaxis in a Patient with Alcoholic Cirrhosis
Akhtar, E., Parikh, D., & Torok, N. (2013). Calciphylaxis in a Patient with Alcoholic Cirrhosis. AMERICAN JOURNAL OF GASTROENTEROLOGY, 108, S337. -
Nox4 plays an important role in alcohol-induced hepatic oxidative stress
Chen, X., Jiang, J., Fukada, H., Schroder, K., Brandes, R. P., & Torok, N. (2012). Nox4 plays an important role in alcohol-induced hepatic oxidative stress. HEPATOLOGY, 56, 1124A. -
NADPH oxidase 4 plays a key role in hepatocyte injury and HSC activation leading to NASH progression
Jiang, J., Chen, X., Fukada, H., Schroder, K., Brandes, R. P., Devaraj, S., & Torok, N. (2012). NADPH oxidase 4 plays a key role in hepatocyte injury and HSC activation leading to NASH progression. HEPATOLOGY, 56, 258A. -
NOX4 IS A KEY ENZYME IN ALCOHOLIC LIVER DISEASE
Chen, X., Fukada, H., Jiang, X., & Torok, N. J. (2012). NOX4 IS A KEY ENZYME IN ALCOHOLIC LIVER DISEASE. ALCOHOLISM-CLINICAL AND EXPERIMENTAL RESEARCH, 36, 76A. -
NOX4 INDUCTION IS ATTENUATED IN NOX2-/- MICE DURING LIVER FIBROSIS
Chen, X., Jiang, X., Serizawa, N., & Torok, N. (2011). NOX4 INDUCTION IS ATTENUATED IN NOX2-/- MICE DURING LIVER FIBROSIS. HEPATOLOGY, 54, 739A–740A. -
TREATMENT WITH A NOVEL NOX4 INHIBITOR ATTENUATES LIVER FIBROSIS
Chen, X., Jiang, X., Serizawa, N., Szyndralewiez, C., Page, P., & Torok, N. (2011). TREATMENT WITH A NOVEL NOX4 INHIBITOR ATTENUATES LIVER FIBROSIS. HEPATOLOGY, 54, 740A. -
ADVANCED GLYCATION END PRODUCTS INDUCE INFLAMMATORY AND FIBROGENIC ACTIVITY IN NASH BY REGULATING TIMP3/TACE ACTIVITY
Jiang, X., Chen, X., Serizawa, N., & Torok, N. (2011). ADVANCED GLYCATION END PRODUCTS INDUCE INFLAMMATORY AND FIBROGENIC ACTIVITY IN NASH BY REGULATING TIMP3/TACE ACTIVITY. HEPATOLOGY, 54, 735A. -
PHAGOCYTOSIS OF APOPTOTIC CELLS BY HEPATIC STELLATE CELLS INDUCES CD8+PROLIFERATION AND ACTIVATION IN VITRO AND IN VIVO
Jiang, J., Serizawa, N., Chen, X., Murphy, W. J., Ames, E., Ma, W., & Torok, N. (2010). PHAGOCYTOSIS OF APOPTOTIC CELLS BY HEPATIC STELLATE CELLS INDUCES CD8+PROLIFERATION AND ACTIVATION IN VITRO AND IN VIVO. HEPATOLOGY, 52(4), 1263A. -
GALECTIN 3 INDUCES HCC INVASIVENESS BY A RHOA AND MLCK MEDIATED PATHWAY
Serizawa, N., Jiang, J., Chen, X., & Torok, N. (2010). GALECTIN 3 INDUCES HCC INVASIVENESS BY A RHOA AND MLCK MEDIATED PATHWAY. HEPATOLOGY, 52(4), 952A–953A. -
GALECTIN 3 IS A SURVIVAL PROTEIN AND PLAYS A ROLE IN THE DEVELOPMENT OF HCC IN MICE
Jiang, J., Scott, F., Li, Y., Serizawa, N., Devaraj, S., Hsu, D. K., … Torok, N. (2009). GALECTIN 3 IS A SURVIVAL PROTEIN AND PLAYS A ROLE IN THE DEVELOPMENT OF HCC IN MICE. HEPATOLOGY, 50(4), 854A. -
SOLUBLE LEPTIN RECEPTOR CORRELATES WITH THE STATE OF INSULIN RESISTANCE AND ADVANCED FIBROSIS IN NAFLD/NASH
Medici, V., Aoki, C., Ali, M., Jiang, J., Havel, P. J., Seo, S., … Torok, N. (2008). SOLUBLE LEPTIN RECEPTOR CORRELATES WITH THE STATE OF INSULIN RESISTANCE AND ADVANCED FIBROSIS IN NAFLD/NASH. HEPATOLOGY, 48(4), 520A–521A. -
Macrophage Nourishment in NASH: A Novel Role for Ketone Bodies.
Torok, N. J. (2019). Macrophage Nourishment in NASH: A Novel Role for Ketone Bodies. Hepatology (Baltimore, Md.). -
SHC MODULATES OXIDATIVE AND INFLAMMATORY SIGNALS IN ALCOHOLIC LIVER DISEASE
Dehnad, A., Das, S., Fish, S. R., Jiang, J. X., & Torok, N. J. (2019). SHC MODULATES OXIDATIVE AND INFLAMMATORY SIGNALS IN ALCOHOLIC LIVER DISEASE. ALCOHOLISM-CLINICAL AND EXPERIMENTAL RESEARCH, 43, 46A. -
Patterns and co-occurrence of risk factors for hepatocellular carcinoma in four Asian American communities: a cross-sectional study.
Stewart, S. L., Dang, J. H., Torok, N. J., & Chen, M. S. (2019). Patterns and co-occurrence of risk factors for hepatocellular carcinoma in four Asian American communities: a cross-sectional study. BMJ Open, 9(6), e026409. -
Digoxin improves steatohepatitis with differential involvement of liver cell subsets in mice through inhibition of PKM2 transactivation.
Zhao, P., Han, S.-N., Arumugam, S., Yousaf, M. N., Qin, Y., Jiang, J. X., … Ouyang, X. (2019). Digoxin improves steatohepatitis with differential involvement of liver cell subsets in mice through inhibition of PKM2 transactivation. American Journal of Physiology. Gastrointestinal and Liver Physiology. -
SHC LINKS OXIDATIVE AND INFLAMMATORY SIGNALS IN ALCOHOLIC LIVER DISEASE (ALD)
Gupta, P., Dehnad, A., Das, S., Fish, S., Jiang, J. X., Cortopassi, G., & Torok, N. J. (2019). SHC LINKS OXIDATIVE AND INFLAMMATORY SIGNALS IN ALCOHOLIC LIVER DISEASE (ALD). HEPATOLOGY. WILEY. -
Leptin/adiponectin ratio correlates with hepatic steatosis but not arterial stiffness in nonalcoholic fatty liver disease in Japanese population.
Mikami, K., Endo, T., Sawada, N., Igarashi, G., Kimura, M., Hasegawa, T., … Fukuda, S. (2019). Leptin/adiponectin ratio correlates with hepatic steatosis but not arterial stiffness in nonalcoholic fatty liver disease in Japanese population. Cytokine, 126, 154927. -
Non-phagocytic Activation of NOX2 is Implicated in Progressive Non-alcoholic Steatohepatitis During Aging.
Jiang, J. X., Fish, S. R., Tomilov, A., Li, Y., Fan, W., Dehnad, A., … Török, N. J. (2020). Non-phagocytic Activation of NOX2 is Implicated in Progressive Non-alcoholic Steatohepatitis During Aging. Hepatology (Baltimore, Md.). -
AGER1 downregulation associates with fibrosis in nonalcoholic steatohepatitis and type 2 diabetes.
Dehnad, A., Fan, W., Jiang, J. X., Fish, S. R., Li, Y., Das, S., … Török, N. J. (2020). AGER1 downregulation associates with fibrosis in nonalcoholic steatohepatitis and type 2 diabetes. The Journal of Clinical Investigation. -
Soluble epoxide hydrolase hepatic deficiency ameliorates alcohol-associated liver disease.
Mello, A., Hsu, M.-F., Koike, S., Chu, B., Cheng, J., Yang, J., … Haj, F. G. (2020). Soluble epoxide hydrolase hepatic deficiency ameliorates alcohol-associated liver disease. Cellular and Molecular Gastroenterology and Hepatology. -
THE INCIDENCE OF HEPATOCELLULAR CARCINOMA IN CHRONIC HEPATITIS B VIRUS INFECTION SUBJECTS NOT MEETING CRITERIA FOR ANTIVIRAL THERAPY
Alshuwaykh, O., Goel, A., Daugherty, T., Cheung, A., Kim, W. R., Kwong, A. J., … Kwo, P. Y. (2020). THE INCIDENCE OF HEPATOCELLULAR CARCINOMA IN CHRONIC HEPATITIS B VIRUS INFECTION SUBJECTS NOT MEETING CRITERIA FOR ANTIVIRAL THERAPY. HEPATOLOGY. WILEY. -
SHC INHIBITORY DRUG IDEBENONE PROTECTS MICE FROM DIET-INDUCED NASH
Jiang, J. X., Tomilov, A., Torok, N. J., & Cortopassi, G. (2020). SHC INHIBITORY DRUG IDEBENONE PROTECTS MICE FROM DIET-INDUCED NASH. HEPATOLOGY, 72, 1036–37. -
NADPH oxidase 4 (Nox4) deletion accelerates liver regeneration in mice
Herranz-Iturbide, M., Lopez-Luque, J., Gonzalez-Sanchez, E., Caballero-Diaz, D., Crosas-Molist, E., Martin-Mur, B., … Fabregat, I. (2021). NADPH oxidase 4 (Nox4) deletion accelerates liver regeneration in mice. FREE RADICAL BIOLOGY AND MEDICINE, 165. -
Editorial: Noninvasive Fibrosis Biomarkers in Patients With NASH With Diabetes.
Fan, W., & Torok, N. J. (2021). Editorial: Noninvasive Fibrosis Biomarkers in Patients With NASH With Diabetes. Hepatology Communications, 5(4), 553–55. -
Phagocytosis of apoptotic bodies by human stellate cells induces NADPH oxidase activation.
Torok, N. J., Wu, J., Zern, M. A., Friedman, S. L., & Zhan, S. S. (2004). Phagocytosis of apoptotic bodies by human stellate cells induces NADPH oxidase activation. HEPATOLOGY, 40(4), 532A–533A. -
Non-alcoholic Fatty Liver Disease and Liver Fibrosis during Aging
Li, Y., Adeniji, N. T., Fan, W., Kunimoto, K., & Torok, N. J. (2022). Non-alcoholic Fatty Liver Disease and Liver Fibrosis during Aging. AGING AND DISEASE. -
Shc is implicated in calreticulin-mediated sterile inflammation in alcoholic hepatitis.
Li, Y., Jiang, J. X., Fan, W., Fish, S. R., Das, S., Gupta, P., … Torok, N. J. (2022). Shc is implicated in calreticulin-mediated sterile inflammation in alcoholic hepatitis. Cellular and Molecular Gastroenterology and Hepatology. -
Primary sclerosing cholangitis and the path to translation.
Váncza, L., & Torok, N. J. (2023). Primary sclerosing cholangitis and the path to translation. The Journal of Clinical Investigation, 133(17). -
Matrix viscoelasticity promotes liver cancer progression in the pre-cirrhotic liver.
Fan, W., Adebowale, K., Váncza, L., Li, Y., Rabbi, M. F., Kunimoto, K., … Török, N. J. (2024). Matrix viscoelasticity promotes liver cancer progression in the pre-cirrhotic liver. Nature. -
Metabolic dysfunction-associated liver disease and diabetes: Matrix remodeling, fibrosis, and therapeutic implications.
Fan, W., Bradford, T. M., & Török, N. J. (2024). Metabolic dysfunction-associated liver disease and diabetes: Matrix remodeling, fibrosis, and therapeutic implications. Annals of the New York Academy of Sciences. -
ECM1 attenuates hepatic fibrosis by interfering with mediators of latent TGF-ß1 activation.
Link, F., Li, Y., Zhao, J., Munker, S., Fan, W., Nwosu, Z. C., … Wang, S. (2024). ECM1 attenuates hepatic fibrosis by interfering with mediators of latent TGF-ß1 activation. Gut.
-
Ductular reaction-on-a-chip: Microfluidic co-cultures to study stem cell fate selection during liver injury
Clinical Trials
Clinical trials are research studies that evaluate a new medical approach, device, drug, or other treatment. As a Stanford Health Care patient, you may have access to the latest, advanced clinical trials.
Open trials refer to studies currently accepting participants. Closed trials are not currently enrolling, but may open in the future.
Practice Locations
Liver Transplant Program at Boswell Building Stanford, CA
Stanford, CALiver Transplant Program at Boswell Building
300 Pasteur Drive
Stanford , CA 94305
Make An Appointment More Clinic Information Getting HereLiver (Hepatology) Clinic in Redwood City Redwood City, CA
Redwood City, CALiver (Hepatology) Clinic in Redwood City
420 Broadway Street, Pavilion D, 2nd Floor
Redwood City , CA 94063
Make An Appointment More Clinic Information Getting HereDigestive Health Center in Redwood City Redwood City, CA
Redwood City, CADigestive Health Center in Redwood City
420 Broadway Street, Pavilion D, 2nd Floor
Redwood City , CA 94063
Make An Appointment More Clinic Information Getting HereAdvanced Endoscopy in Palo Alto Stanford, CA
Stanford, CAAdvanced Endoscopy in Palo Alto
300 Pasteur Drive, Ground Floor
Stanford , CA 94305
Make An Appointment More Clinic Information Getting HereImportant Information about Our Organizations and Physician Affiliation
Stanford Health Care, Stanford Health Care Tri-Valley, and Stanford Medicine Partners are each independent nonprofit organizations that are affiliated with but separate from each other and from Stanford University. The physicians who provide care at facilities operated by Stanford Health Care, Stanford Health Care Tri-Valley, and Stanford Medicine Partners are faculty, foundation, or community physicians who are not employees, representatives, or agents of Stanford Health Care, Stanford Health Care Tri- Valley, or Stanford Medicine Partners. Stanford Health Care, Stanford Health Care Tri-Valley, and Stanford Medicine Partners do not exercise control over the care provided by such faculty, foundation, and community physicians and are not responsible for their actions.
Patient Reviews
(28 reviews)
View More
Referring Physicians
PHYSICIAN HELPLINE
Fax: 650-320-9443
Monday–Friday, 8 a.m.–5 p.m.
Stanford Health Care provides comprehensive services to refer and track patients, as well as the latest information and news for physicians and office staff. For help with all referral needs and questions, visit Referral Information.
You may also submit a web referral or complete a referral form and fax it to 650-320-9443 or email the Referral Center at ReferralCenter@stanfordhealthcare.org.
- Send referrals online
- Place radiology and lab orders
- View referral status
- Access medical records