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Non coding RNA and Intercellular Communication in Cardiac Ageing

Life expectancy in the European Union is rising and the prevalence of age-induced cardiovascular disease increases concomitantly. The main clinical presentation of age-induced cardiovascular disease is heart failure with preserved... ver más

31/03/2026

STICHTING AMSTERDA...

2M€

Presupuesto del proyecto: 2M€

Líder del proyecto

STICHTING AMSTERDAM UMC No se ha especificado una descripción o un objeto social para esta compañía.

TRL 4-5

Fecha límite participación Sin fecha límite de participación.

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Financiación concedida El organismo H2020 notifico la concesión del proyecto el día 2021-03-05

ERC-2020-COG: ERC CONSOLIDATOR GRANTS

I+D

Cerrada hace 4 años

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2 Participantes

STICHTING AMSTERDAM UMC

2.00M€ | Lider

BSH ELECTRODOMESTICOS ESPAÑA

1.59M€ | Participante

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Duración del proyecto: 60 meses Fecha Inicio: 2021-03-05
Fecha Fin: 2026-03-31

Líder del proyecto

STICHTING AMSTERDAM UMC No se ha especificado una descripción o un objeto social para esta compañía.

TRL 4-5

Presupuesto del proyecto 2M€

Fecha límite de participación Sin fecha límite de participación.

Descripción del proyecto Life expectancy in the European Union is rising and the prevalence of age-induced cardiovascular disease increases concomitantly. The main clinical presentation of age-induced cardiovascular disease is heart failure with preserved ejection fraction (HFpEF). HFpEF is a complex disease involving different cell types and mechanisms that contribute to impaired relaxation of cardiomyocytes. Currently there is no appropriate treatment for HFpEF. This proposal aims to better understand the molecular mechanisms behind intercellular communication and ageing that lead to HFpEF. Long non-coding RNAs (lncRNAs) are emerging as novel key regulators of cellular functions and we hypothesize that lncRNAs contribute to ageing-induced cardiac dysfunction, including HFpEF. Preliminary experiments show that several long non-coding RNAs (lncRNAs) are differentially regulated during cardiac ageing, including the cardiomyocyte-enriched lncRNA Sarrah that is essential for cardiomyocyte survival. We propose to extensively characterize the role of Sarrah in HFpEF and to identify other lncRNAs that are involved in cardiac ageing. Importantly, we will focus those lncRNAs that are also affected in a cohort of human HFpEF patients. Furthermore, since disturbed intercellular communication is a hallmark of both ageing and HFpEF, we will identify lncRNAs that regulate endothelial cell-cardiomyocyte crosstalk. We will use state-of-the-art in vitro and in vivo models to assess cardiac ageing and function upon gain-of-function and loss-of-function of lncRNAs in a cell-type specific manner. Understanding the role that Sarrah and other lncRNAs play in cardiac ageing and HFpEF will highlight novel potential therapeutic targets to attenuate age-induced cardiac dysfunction and will increase our knowledge of the underlying mechanisms controlling intercellular communication and cardiac function.

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