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MacinNASH SIGNED

Revealing the contribution of liver macrophage populations to NASH in insulin resistance

Total Cost €

0

EC-Contrib. €

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Partnership

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Project "MacinNASH" data sheet

The following table provides information about the project.

Coordinator
KAROLINSKA INSTITUTET 

Organization address
address: Nobels Vag 5
city: STOCKHOLM
postcode: 17177
website: www.ki.se

contact info
title: n.a.
name: n.a.
surname: n.a.
function: n.a.
email: n.a.
telephone: n.a.
fax: n.a.

 Coordinator Country Sweden [SE]
 Total cost 1˙999˙781 €
 EC max contribution 1˙999˙781 € (100%)
 Programme 1. H2020-EU.1.1. (EXCELLENT SCIENCE - European Research Council (ERC))
 Code Call ERC-2019-COG
 Funding Scheme ERC-COG
 Starting year 2020
 Duration (year-month-day) from 2020-03-01   to  2025-02-28

 Partnership

Take a look of project's partnership.

# participants  country  role  EC contrib. [€] 
1    KAROLINSKA INSTITUTET SE (STOCKHOLM) coordinator 1˙999˙781.00

Map

 Project objective

Non-alcoholic steatohepatitis (NASH), the most common chronic liver disease worldwide, is an unmet medical need with no approved therapies and debilitating consequences for patients. Obesity-associated insulin resistance is a high-risk factor for the development of NASH. The prevailing paradigm is a multiple hit process, whereby lipid accumulation in the liver of obese patients leads to oxidative stress and increased production of inflammatory cytokines by macrophages. However, my research group's comprehensive investigations in mice and humans have revealed that liver macrophages (LMs) contribute to insulin resistance and oxidative stress independently of their inflammatory status. I thereby propose that LMs predispose insulin resistant patients to NASH independently of their inflammatory status.  In this ambitious multidisciplinary project, we will use a novel platform encompassing multiple single cell and in situ omics technologies tailored by my research group to characterize the phenotype of LM populations in healthy individuals and insulin resistant patients with or without NASH. We will strengthen this approach with functional validation in animal models as well as human liver organoids using a patented technology that I have developed to specifically manipulate gene expression in macrophages. We will then decipher how hepatic insulin resistance creates a spatiotemporal environment facilitating NASH. My group's unique access to patient material combined with cutting-edge methodologies to reveal the phenotype of single LMs provides an exceptional starting point from which to identify genes and pathways involved in the development of NASH in obese insulin resistant patients. This project will set the stage for a paradigm-shift in studying and treating life-threatening liver diseases.

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The information about "MACINNASH" are provided by the European Opendata Portal: CORDIS opendata.

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