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CM TURNOVER

Financiado

Cerrado

Uncovering the Mechanisms of Cardiomyocyte Differentiation and Dedifferentiation

The quest to restore damaged organs is one of the major challenges in medicine. Recent studies in both animals and in humans suggest that the heart has a limited capacity to replenish its own cardiomyocytes (CMs) throughout life,... ver más

31/12/2016

WEIZMANN

2M€

Presupuesto del proyecto: 2M€

Líder del proyecto

WEIZMANN INSTITUTE OF SCIENCE No se ha especificado una descripción o un objeto social para esta compañía.

TRL 4-5

Fecha límite participación Sin fecha límite de participación.

Financiación concedida El organismo FP7 notifico la concesión del proyecto el día 2016-12-31 No tenemos la información de la convocatoria

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1 Participantes

WEIZMANN

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Líder del proyecto

WEIZMANN INSTITUTE OF SCIENCE 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 The quest to restore damaged organs is one of the major challenges in medicine. Recent studies in both animals and in humans suggest that the heart has a limited capacity to replenish its own cardiomyocytes (CMs) throughout life, albeit inadequate to compensate for major injuries such as acute myocardial infarction (MI). Most therapeutic research in regenerative cardiogenesis is geared toward stem cell therapy as a means to replace lost CMs associated with ischemic heart disease. Clinical data evaluating the efficacy of cell-based therapy for heart disease are relatively disappointing. This proposal encompasses multidisciplinary and novel approaches to study the molecular and cellular mechanisms that govern the proliferation, differentiation and dedifferentiation of endogenous CMs, combining developmental-, systems- and cell-biology methodologies in vitro and in vivo, in chick, rodent, and human tissue samples. First, we will perform combinatorial perturbations of signaling pathways in chick embryos, focusing primarily on the FGF-ERK pathway, to investigate the molecular switch between cardiac progenitors and CMs (Aim 1). Because adult CMs have limited proliferative capacity, mainly due to mechanical constraints, in Aim 2, we will apply state-of-the-art techniques in cell biology, to determine whether specific mechno-transduction stimuli can prime the proliferation of differentiated CMs. In order to gain deeper insights into the capacity of adult CMs to renew themselves under normal and pathological conditions, in Aim 3, we will employ a novel cell lineage methodology in mouse and human tissue, based on information encoded in genome. Using this methodology, we hope to shed light on the maintenance, renewal and regenerative capacities of adult CMs in vivo. The expected outcome will be a significantly greater understanding of the bidirectional transition from proliferating cardiac progenitors into differentiated CMs, in embryonic and adult hearts.

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