Summary
Liver fibrosis is increasing in prevalence in many Western populations (mainly due to alcoholic liver disease and non-alcoholic fatty liver disease) and has a major burden on care provision as to date there is no specific intervention to reverse fibrosis. One of the factors that could regulate liver fibrosis is the intestinal microbiome, as various microbial derived compounds reach the liver through the portal vein and act on the liver cells including stellate and Kupffer cells, the main drivers of liver fibrosis. My hypothesis is that the hepatic stellate cells phenotype could be driven by the microbiome and microbial derived metabolites. The key objective is to gain comprehensive understanding on how the microbiome modifies liver homoeostasis and contribute to liver fibrosis development using analysis of the network perturbation in disease, coupled with microbiome experimental techniques. To achieve this, I plan to answer three main questions: 1) which microbiome states and microbiome derived metabolite modulate fibrosis; 2) how does these microbiome states and metabolites changes the hepatic stellate cells phenotype at a cellular and spatial level; 3) which are the mechanisms by which the microbiome modulates liver fibrosis. This will allow characterizing in depth and dissecting the molecular mechanisms of fibrosis and the contribution of microbiome and microbial associated products. Furthermore, identification of potential factors affecting the course of the disease may lead to potential assisting therapies involving the microbiome and at term leading to an improvement in the prognostic and management of patients with liver fibrosis.
The Marie Skłodowska-Curie Fellowship is an important point in my career because it will allow me to ask relevant and innovative questions about host–microbe interactions, learn new approaches and transition from being a physician to an early career physician-scientist and a research group leader.
The Marie Skłodowska-Curie Fellowship is an important point in my career because it will allow me to ask relevant and innovative questions about host–microbe interactions, learn new approaches and transition from being a physician to an early career physician-scientist and a research group leader.
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More information & hyperlinks
| Web resources: | https://cordis.europa.eu/project/id/101068605 |
| Start date: | 01-06-2022 |
| End date: | 31-05-2024 |
| Total budget - Public funding: | - 184 698,00 Euro |
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Original description
Liver fibrosis is increasing in prevalence in many Western populations (mainly due to alcoholic liver disease and non-alcoholic fatty liver disease) and has a major burden on care provision as to date there is no specific intervention to reverse fibrosis. One of the factors that could regulate liver fibrosis is the intestinal microbiome, as various microbial derived compounds reach the liver through the portal vein and act on the liver cells including stellate and Kupffer cells, the main drivers of liver fibrosis. My hypothesis is that the hepatic stellate cells phenotype could be driven by the microbiome and microbial derived metabolites. The key objective is to gain comprehensive understanding on how the microbiome modifies liver homoeostasis and contribute to liver fibrosis development using analysis of the network perturbation in disease, coupled with microbiome experimental techniques. To achieve this, I plan to answer three main questions: 1) which microbiome states and microbiome derived metabolite modulate fibrosis; 2) how does these microbiome states and metabolites changes the hepatic stellate cells phenotype at a cellular and spatial level; 3) which are the mechanisms by which the microbiome modulates liver fibrosis. This will allow characterizing in depth and dissecting the molecular mechanisms of fibrosis and the contribution of microbiome and microbial associated products. Furthermore, identification of potential factors affecting the course of the disease may lead to potential assisting therapies involving the microbiome and at term leading to an improvement in the prognostic and management of patients with liver fibrosis.The Marie Skłodowska-Curie Fellowship is an important point in my career because it will allow me to ask relevant and innovative questions about host–microbe interactions, learn new approaches and transition from being a physician to an early career physician-scientist and a research group leader.
Status
SIGNEDCall topic
HORIZON-MSCA-2021-PF-01-01Update Date
09-02-2023
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