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MacinNASH

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Revealing the contribution of liver macrophage populations to NASH in insulin re...

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

28/02/2025

2M€

Presupuesto del proyecto: 2M€

Líder del proyecto

KAROLINSKA INSTITUTET No se ha especificado una descripción o un objeto social para esta compañía.

TRL 4-5

Ver 2 Participantes

Financiación concedida El organismo H2020 notifico la concesión del proyecto el día 2020-02-14

ERC-2019-COG: ERC Consolidator Grant

I+D

Cerrada hace 5 años

0% 100% 100%

2 Participantes

2.00M€ | Lider

TAHE PRODUCTOS COSMETICOS

419.50K€ | Participante

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Duración del proyecto: 60 meses Fecha Inicio: 2020-02-14
Fecha Fin: 2025-02-28

Líder del proyecto

KAROLINSKA INSTITUTET No se ha especificado una descripción o un objeto social para esta compañía.

TRL 4-5

Presupuesto del proyecto 2M€

Descripción del proyecto 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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