ZEBRAHEART
Novel insights into cardiac regeneration through studies in the zebrafish
| Coordinatore | UNIVERSITAET BERN
Spiacenti, non ci sono informazioni su questo coordinatore. Contattare Fabio per maggiori infomrazioni, grazie. |
| Nazionalità Coordinatore | Switzerland [CH] |
| Totale costo | 1˙499˙215 € |
| EC contributo | 1˙499˙215 € |
| 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-2013-StG |
| Funding Scheme | ERC-SG |
| Anno di inizio | 2014 |
| Periodo (anno-mese-giorno) | 2014-02-01 - 2019-01-31 |
Partecipanti
| # | ||||
|---|---|---|---|---|
| 1 |
FUNDACION CENTRO NACIONAL DE INVESTIGACIONES CARDIOVASCULARES CARLOS III
Organization address
address: C/ MELCHOR FERNANDEZ ALMAGRO 3 contact info |
ES (MADRID) | beneficiary | 476˙725.98 |
| 2 |
UNIVERSITAET BERN
Organization address
address: Hochschulstrasse 4 contact info |
CH (BERN) | hostInstitution | 1˙022˙489.02 |
| 3 |
UNIVERSITAET BERN
Organization address
address: Hochschulstrasse 4 contact info |
CH (BERN) | hostInstitution | 1˙022˙489.02 |
Mappa
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Obiettivo del progetto (Objective)
Myocardial infarction (MI) leads to cardiomyocyte death and accumulation of myofibroblasts (MFs) at the site of injury, which produce large amounts of extracellular matrix (ECM), generating a scar. Initially, cardiac fibrosis protects from ventricular wall rupture, but subsequent myocardial remodelling causes heart failure, representing a leading cause of death in Europe. While MFs play a central role in cardiac fibrosis, there is confusion on their origin, a lack of specific markers and the existence of a unique MF type is debatable. Different MF might reveal distinct characteristics regarding ECM production, contractility, and autophagy, making them more or less pernicious. While in humans cardiac fibrosis is irreversible, other vertebrates have a remarkable capacity to regenerate damaged tissue. We recently established a zebrafish MI model and found that cardiac fibrosis is reversible and occurs as an intermediate step during regeneration. Here, the endogenous mechanisms of MFs and ECM regression will be explored. In addition, MF origin, types and fate will be characterized and manipulated to improve regeneration. As in mammals, cardiac injury elicits an inflammatory response in the zebrafish. The regenerative capacity of a species has been directly linked to features of its immune system, but surprisingly little is known on zebrafish leukocyte subtypes. We will study the role of macrophages and particularly analyse a subtype, which accumulates in the outer mesothelial layer of the heart, the epicardium. Epicardial derived cells play a key role as a trophic factor and progenitor cell source, and a first step towards regeneration includes the reestablishment of the epicardial layer. The zebrafish will offer a screening platform for small molecules triggering its activation. In sum, the project will increase the knowledge on the molecular and cellular basis of fibrosis regression, provide novel MF markers and identify new drugs to enhance cardiac regeneration.