CM TURNOVER

Uncovering the Mechanisms of Cardiomyocyte Differentiation and Dedifferentiation

 Coordinatore WEIZMANN INSTITUTE OF SCIENCE 

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 Nazionalità Coordinatore Israel [IL]
 Totale costo 1˙500˙000 €
 EC contributo 1˙500˙000 €
 Programma FP7-IDEAS-ERC
Specific programme: "Ideas" implementing the Seventh Framework Programme of the European Community for research, technological development and demonstration activities (2007 to 2013)
 Code Call ERC-2011-StG_20101109
 Funding Scheme ERC-SG
 Anno di inizio 2012
 Periodo (anno-mese-giorno) 2012-01-01   -   2016-12-31

 Partecipanti

# participant  country  role  EC contrib. [€] 
1    WEIZMANN INSTITUTE OF SCIENCE

 Organization address address: HERZL STREET 234
city: REHOVOT
postcode: 7610001

contact info
Titolo: Ms.
Nome: Gabi
Cognome: Bernstein
Email: send email
Telefono: +972 8 934 6728
Fax: +972 8 934 4165

IL (REHOVOT) hostInstitution 1˙500˙000.00
2    WEIZMANN INSTITUTE OF SCIENCE

 Organization address address: HERZL STREET 234
city: REHOVOT
postcode: 7610001

contact info
Titolo: Prof.
Nome: Eldad
Cognome: Tzahor
Email: send email
Telefono: +972 8 934 3715
Fax: +972 8 934 4116

IL (REHOVOT) hostInstitution 1˙500˙000.00

Mappa


 Word cloud

Esplora la "nuvola delle parole (Word Cloud) per avere un'idea di massima del progetto.

limited    chick    capacity    human    therapy    disease    cardiac    tissue    regenerative    cms    biology    methodology    adult    molecular    vivo    differentiated    cell    heart    proliferation    progenitors   

 Obiettivo del progetto (Objective)

'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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