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iPROTECTION

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Molecular mechanisms of induced protection against sepsis by DNA damage response...

Severe sepsis remains a poorly understood systemic inflammatory condition with high mortality rates and limited therapeutic options outside of infection control and organ support measures. Based on our recent discovery that anthra... ver más

31/03/2021

FUNDACAO CALOUSTE...

2M€

Presupuesto del proyecto: 2M€

Líder del proyecto

FUNDACAO CALOUSTE GULBENKIAN 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 2021-03-31

Línea de financiación objetivo El proyecto se financió a través de la siguiente ayuda:

ERC-CoG-2014: ERC Consolidator Grant

I+D

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2 Participantes

FUNDACAO CALOUSTE GULBENKIAN

1.99M€ | Lider

CAFENTO COFFEE FACTORY

267.77K€ | Participante

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27-11-2024: DGIPYME En las últimas 48 horas el Organismo DGIPYME ha otorgado 1 concesiones

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Duración del proyecto: 67 meses Fecha Inicio: 2015-08-31
Fecha Fin: 2021-03-31

Líder del proyecto

FUNDACAO CALOUSTE GULBENKIAN

TRL 4-5

Presupuesto del proyecto 2M€

Descripción del proyecto Severe sepsis remains a poorly understood systemic inflammatory condition with high mortality rates and limited therapeutic options outside of infection control and organ support measures. Based on our recent discovery that anthracycline drugs prevent organ failure without affecting the bacterial burden in a model of severe sepsis, we propose that strategies aimed at target organ protection have extraordinary potential for the treatment of sepsis and possibly for other inflammation-driven conditions. However, the mechanisms of organ protection and disease tolerance are either unknown or poorly characterized. The central goal of the current proposal is to identify and characterize novel cytoprotective mechanisms, with a focus on DNA damage response dependent protection activated by anthracyclines as a window into stress-induced genetic programs conferring disease tolerance. To that end, we will carry out a combination of candidate and unbiased approaches for the in vivo identification of ATM-dependent and independent mechanisms of tissue protection. We will validate the leading candidates through adenovirus-mediated delivery of constructs for overexpression (gain-of-function) or shRNA for gene silencing (loss-of-function) to the lung, based on our recent finding that rescuing this organ is essential and perhaps sufficient in anthracycline-induced protection against severe sepsis. The candidates showing the most promise will be characterized using a combination of in vitro and in vivo genetic, biochemical, cell biological and physiological methods. The results arising from the current proposal are likely not only to inspire the design of transformative therapies for sepsis but also to open a completely new field of opportunity to molecularly understand core surveillance mechanisms of basic cellular processes with a critical role in the homeostasis of organ function and whose activation can ultimately promote quality of life during aging and increase lifespan.

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