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EXpansion and Phenotype Loss Of SMCs In Atherosclerosis Causal effects and ther...

EXpansion and Phenotype Loss Of SMCs In Atherosclerosis Causal effects and therapeutic possibilities Atherosclerosis is considered an inflammatory disease caused by the accumulation, modification and immune cell recognition of low-density lipoproteins in the arterial wall. Plaque macrophages are held to be the main drivers of dis... see more

31/07/2025

2M€

Project Budget: 2M€

Project leader

AARHUS UNIVERSITET No se ha especificado una descripción o un objeto social para esta compañía.

TRL 4-5

PARTICIPATION DEPralty Sin fecha límite de participación.

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Financing granted El organismo H2020 notifico la concesión del proyecto The day 2025-07-31

ERC-2019-COG: ERC Consolidator Grant Scope:Objectives

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Cerrada does 6 years

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characteristics of the participant

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

Private Information

No hay información privada compartida para este proyecto. Habla con el coordinador.

3 Participantes

1.30M€ | Leader

CONSULTORES PARA LA DIFUSION...

176.58K€ | participant

CENTRO NACIONAL DE INVESTIGA...

702.76K€ | participant

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Project duration: 64 months Date Start: 2020-03-02
End date: 2025-07-31

Project leader

AARHUS UNIVERSITET No se ha especificado una descripción o un objeto social para esta compañía.

TRL 4-5

Project Budget 2M€

participation deadline Sin fecha límite de participación.

Project description Atherosclerosis is considered an inflammatory disease caused by the accumulation, modification and immune cell recognition of low-density lipoproteins in the arterial wall. Plaque macrophages are held to be the main drivers of disease activity, whereas smooth muscle cells (SMCs) have traditionally been considered protective by forming fibrous tissue that stabilises plaques from undergoing rupture and causing thrombosis. In the present project, we challenge this dichotomous view of cellular villains and heroes in atherosclerosis. Using lineage tracking techniques in mice, we and others have uncovered a large population of SMCs in plaques, which has escaped detection because the cells completely lose conventional SMC phenotype. Strikingly, we have found that the entire plaque SMC population derives from only few founder SMCs that undergo massive clonal expansion and phenotypic modulation during lesion formation. We hypothesise that the balance between the different modulated SMC subtypes and the functions they carry are central to lesion progression. In EXPLOSIA we will address this hypothesis in 3 steps. First, we will conduct a comparative analysis of clonal structure in mice, minipigs, and humans. Second, we will determine links between SMC subtypes, their gene expression programs, and atherosclerotic disease activity by combining single-cell transcriptomics with novel techniques to alter atherosclerotic disease activity in gene-modified mice and minipigs. Third, we will develop techniques for manipulating genes in modulated plaque SMCs and test the causal role of perturbing SMC subtypes and function for lesion progression. The aim of the project is to answer the following key questions for a deeper understanding of atherosclerosis: - What is the clonal architecture of SMCs in human atherosclerosis? - What is the SMC gene expression signature of atherosclerotic disease activity? - Can interventions targeting SMCs prevent dangerous lesion development?

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