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MICFIB

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MICROBIOME-DRIVERS OF LIVER FIBROSIS

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 interven... see more

31/05/2024

WEIZMANN

185K€

Project Budget: 185K€

Project leader

WEIZMANN INSTITUTE OF SCIENCE No se ha especificado una descripción o un objeto social para esta compañía.

TRL 4-5

PARTICIPATION DEPralty Sin fecha límite de participación.

Financing granted El organismo HORIZON EUROPE notifico la concesión del proyecto The day 2024-05-31

HORIZON-MSCA-2021-PF-01-01: MSCA Postdoctoral Fellowships 2024 ExpectedOutcome:

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characteristics of the participant

Este proyecto no cuenta con búsquedas de partenariado abiertas en este momento.

Private Information

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1 Participantes

WEIZMANN

184.70K€ | Leader

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Project duration: 24 months Date Start: 2022-05-03
End date: 2024-05-31

Project leader

WEIZMANN INSTITUTE OF SCIENCE No se ha especificado una descripción o un objeto social para esta compañía.

TRL 4-5

Project Budget 185K€

participation deadline Sin fecha límite de participación.

Project 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.

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