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Fine tuning the inflammatory response following cardiac injury to promote cardia...

Fine tuning the inflammatory response following cardiac injury to promote cardiac regeneration The pronounced inability of adult human/mammalian heart to regenerate causes millions of deaths following cardiac insult, particularly in the longer term. The extent and persistence of associated inflammation has been generally li... see more

14/03/2023

BIOMEDICAL RESEARC...

153K€

Project Budget: 153K€

Project leader

IDRYMA IATROVIOLOGIKON EREUNON AKADEMIAS ATHI... 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 H2020 notifico la concesión del proyecto The day 2023-03-14

MSCA-IF-2020: Individual Fellowships Objective:The goal of the Individual Fellowships is to enhance the creative and innovative potential...

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

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1 Participantes

BIOMEDICAL RESEARCH FOUNDATI...

153.09K€ | Leader

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Project duration: 24 months Date Start: 2021-02-25
End date: 2023-03-14

Project leader

IDRYMA IATROVIOLOGIKON EREUNON AKADEMIAS ATHI... No se ha especificado una descripción o un objeto social para esta compañía.

TRL 4-5

Project Budget 153K€

participation deadline Sin fecha límite de participación.

Project description The pronounced inability of adult human/mammalian heart to regenerate causes millions of deaths following cardiac insult, particularly in the longer term. The extent and persistence of associated inflammation has been generally linked with adverse cardiac outcomes, including fibrosis, hypertrophy, and dysfunction. However, characteristics of the inflammatory response e.g. the maturity of resident macrophages and/or the activation status of infiltrating cells may differentially influence cardiac fibroblasts and, most importantly, cardiomyocytes, thus affecting cardiac regeneration, hypertrophy, fibrosis and dysfunction. Unraveling crucial parameters of such interactions in appropriate biological systems should confer decisive intervention potential in a serious health problem. In the past years we have studied in detail cellular and molecular players regulating pivotal events initiating or sustaining the progress to heart failure (HF) in mice and zebrafish and we propose here to combine the systems to globally study these interactions.

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