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Leo A. van Grunsven

Researcher at Vrije Universiteit Brussel

Publications -  115
Citations -  9337

Leo A. van Grunsven is an academic researcher from Vrije Universiteit Brussel. The author has contributed to research in topics: Hepatic stellate cell & Fibrosis. The author has an hindex of 38, co-authored 104 publications receiving 7236 citations. Previous affiliations of Leo A. van Grunsven include École normale supérieure de Lyon & Katholieke Universiteit Leuven.

Papers
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Guidelines for the use and interpretation of assays for monitoring autophagy

Daniel J. Klionsky, +1287 more
- 01 Apr 2012 - 
TL;DR: These guidelines are presented for the selection and interpretation of methods for use by investigators who aim to examine macroautophagy and related processes, as well as for reviewers who need to provide realistic and reasonable critiques of papers that are focused on these processes.
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Stellate Cells, Hepatocytes, and Endothelial Cells Imprint the Kupffer Cell Identity on Monocytes Colonizing the Liver Macrophage Niche

Johnny Bonnardel, +22 more
- 15 Oct 2019 - 
TL;DR: It is shown that the Kupffer cell niche is composed of stellate cells, hepatocytes, and endothelial cells that together imprint the liver-specific macrophage identity.
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A role for autophagy during hepatic stellate cell activation.

Lien F R Thoen, +6 more
- 01 Apr 2012 - 
TL;DR: The demonstration of partly inhibition of in vitro HSC activation after treatment with an autophagy inhibitor unveils a potential new therapeutic strategy for liver fibrosis.
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The Hippo pathway effector YAP controls mouse hepatic stellate cell activation

Inge Mannaerts, +9 more
- 01 Sep 2015 - 
TL;DR: YAP activation is a critical driver of hepatic stellate cell activation and inhibition of YAP presents a novel approach for the treatment of liver fibrosis.
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Keratin 19: a key role player in the invasion of human hepatocellular carcinomas

Olivier Govaere, +20 more
- 01 Apr 2014 - 
TL;DR: K19/KRT19 knockdown results in reduced invasion, loss of invadopodia formation and decreased resistance to doxorubicin, 5-fluorouracil and sorafenib, and should be considered as a seperate entity of HCCs.