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Onderzoeker

Leo A van Grunsven

  • Onderzoeksexpertise:

     

    Leo van Grunsven is a developmental biologist (Utrecht, NL) and obtained his PhD in life sciences from the Ecole Normale Supérieure de Lyon (France, 1996). He had his postdoctoral training at the NINDS/NIH (Bethesda, USA, ’96-‘98) and the KU Leuven (Belgium, ’98-‘06) before he moved to the Vrije Universiteit Brussel and became head of the Liver Cell Biology research group in 2009.

    His group studies molecular mechanisms that drive liver homeostasis, fibrosis, and regeneration, with a particular focus on hepatic stellate cells. He also specialized in developing in vitro models for studying chronic liver disease. His group was the first to identify autophagy, AGE- and Hippo-signaling as key mechanisms involved in hepatic stellate cell activation during liver fibrogenesis. His team also reported on the transcriptional changes that are associated with the activation of mouse and human hepatic stellate cells and established the first hepatocyte-injury dependent in vitro liver fibrosis model by using organoid cultures of human hepatocytes and primary or iPSC-derived hepatic stellate cells. The group currently invests in refining and applying their in vitro models of liver fibrosis and investigates the regulation of stress pathways in hepatic stellate cells and other sinusoidal liver cells during an acute and chronic liver injury in mouse models.

  • Trefwoorden:Geneeskunde
  • Disciplines:Hepatologie, Cel-, weefsel- en orgaan engineering
  • Gebruikers van onderzoeksexpertise:

     

    Leo van Grunsven is a developmental biologist (Utrecht, NL) and obtained his PhD in life sciences from the Ecole Normale Supérieure de Lyon (France, 1996). He had his postdoctoral training at the NINDS/NIH (Bethesda, USA, ’96-‘98) and the KU Leuven (Belgium, ’98-‘06) before he moved to the Vrije Universiteit Brussel and became head of the Liver Cell Biology research group in 2009.

    His group studies molecular mechanisms that drive liver homeostasis, fibrosis, and regeneration, with a particular focus on hepatic stellate cells. He also specialized in developing in vitro models for studying chronic liver disease. His group was the first to identify autophagy, AGE- and Hippo-signaling as key mechanisms involved in hepatic stellate cell activation during liver fibrogenesis. His team also reported on the transcriptional changes that are associated with the activation of mouse and human hepatic stellate cells and established the first hepatocyte-injury dependent in vitro liver fibrosis model by using organoid cultures of human hepatocytes and primary or iPSC-derived hepatic stellate cells. The group currently invests in refining and applying their in vitro models of liver fibrosis and investigates the regulation of stress pathways in hepatic stellate cells and other sinusoidal liver cells during an acute and chronic liver injury in mouse models.