Education
- Medical University Lübeck, Germany, 10/1989 - 07/1995
- Harvard Medical School, Boston, MA 08/1995 - 04/1996
- University of Münster, Germany, 05/1996 - 12/1996
- University of Münster, Germany, Department of Pediatrics, Medical Intern, 02/1997 - 07/1998
- University of Münster, Germany, Department of Pediatrics, Medical Resident, 08/1998 - 09/2001
- Oregon Health & Science University, Portland, Oregon, Department of Molecular and Medical Genetics, 10/2001 -10/2005
In the News
Grants and Funding
- Next-generation human liver gene therapy | NIH | 2021-09-30 - 2026-06-30 | Role: Principal Investigator
- Microphysiological systems to interrogate the Islet-Liver-Adipose Axis in normal physiology and Type-2 Diabetes Mellitus | NIH | 2018-09-20 - 2023-07-31 | Role: Co-Principal Investigator
- Targeting AAV vectors to cell types involved in alcohol-induced liver injury | NIH | 2018-09-01 - 2023-05-31 | Role: Principal Investigator
- Building a functional biliary system from hepatocytes | NIH | 2016-09-01 - 2021-07-31 | Role: Co-Principal Investigator
- Microphysiological systems to interrogate the Islet-Liver-Adipose Axis in normal physiology and Type-2 Diabetes Mellitus | NIH | 2018-09-20 - 2020-07-31 | Role: Co-Principal Investigator
- Myofibroblast-to-hepatocyte conversion as a therapy for alcoholic liver disease | NIH | 2013-09-01 - 2016-08-31 | Role: Principal Investigator
- Liver regeneration with stems cells of uniparental origin | NIH | 2008-04-01 - 2013-08-31 | Role: Co-Principal Investigator
Research Narrative
Our research is aimed at developing new therapies for patients with severe liver diseases. To restore liver function in patients with liver failure, we are working on generating hepatocytes from human pluripotent stem cells or by reprogramming of readily accessible human cell types. To be therapeutically effective, these cells need to replicate both function and the ability to proliferate of primary human hepatocytes. To establish and improve protocols for the production of such cells, we have been working on obtaining a detailed molecular understanding of hepatocyte differentiation and regeneration. For this, we are using mouse models for liver cell lineage tracing developed in our laboratory. In addition, we are using rigorous animal models of human liver failure to test the therapeutic efficacy of our surrogate hepatocytes. While developing novel liver cell therapies is our main focus, we are also using hepatocytes derived from human pluripotent stem cells or by reprogramming to generate in vitro and in vivo liver disease models. Another goal of our laboratory is to determine the origin and follow the fate of liver cancer-initiating cells with the goal to identify the molecular mechanisms that drive liver cancer formation and progression. For this, we are using new mouse models generated in our laboratory. By obtaining an improved understanding of hepatocarcinogenesis, we hope to contribute to the development of strategies for early detection and effective eradication of liver cancer.
Research Interests
Liver Regeneration
Liver Cell Therapy
LIver Development
Research Pathways
Publications
- Emerging cell therapy for biliary diseases.| | PubMed
- Transcriptomic Traces of Adult Human Liver Progenitor Cells.| | PubMed
- Broad Distribution of Hepatocyte Proliferation in Liver Homeostasis and Regeneration.| | PubMed
- Hepatocyte Nuclear Factor 4 Alpha Activation Is Essential for Termination of Liver Regeneration in Mice.| | PubMed
- De novo formation of the biliary system by TGFβ-mediated hepatocyte transdifferentiation.| | PubMed
- Postnatal Organogenesis by Transdifferentiation.| | UCSF Research Profile
- Advances in cholangiocarcinoma research: report from the third Cholangiocarcinoma Foundation Annual Conference.| | PubMed
- In Vivo Hepatic Reprogramming of Myofibroblasts with AAV Vectors as a Therapeutic Strategy for Liver Fibrosis.| | PubMed
- Assessing the therapeutic potential of lab-made hepatocytes.| | PubMed
- Physiological ranges of matrix rigidity modulate primary mouse hepatocyte function in part through hepatocyte nuclear factor 4 alpha.| | PubMed