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HepEDOT SIGNED

Conductive, self-doping and biodegradable oligoEDOT-heparin biomaterial for improved electromechanical coupling, cardiac cell retention and delivery of paracrine factors

Total Cost €

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EC-Contrib. €

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Partnership

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 HepEDOT project word cloud

Explore the words cloud of the HepEDOT project. It provides you a very rough idea of what is the project "HepEDOT" about.

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Project "HepEDOT" data sheet

The following table provides information about the project.

Coordinator
IMPERIAL COLLEGE OF SCIENCE TECHNOLOGY AND MEDICINE 

Organization address
address: SOUTH KENSINGTON CAMPUS EXHIBITION ROAD
city: LONDON
postcode: SW7 2AZ
website: http://www.imperial.ac.uk/

contact info
title: n.a.
name: n.a.
surname: n.a.
function: n.a.
email: n.a.
telephone: n.a.
fax: n.a.

 Coordinator Country United Kingdom [UK]
 Total cost 224˙933 €
 EC max contribution 224˙933 € (100%)
 Programme 1. H2020-EU.1.3.2. (Nurturing excellence by means of cross-border and cross-sector mobility)
 Code Call H2020-MSCA-IF-2018
 Funding Scheme MSCA-IF-EF-ST
 Starting year 2019
 Duration (year-month-day) from 2019-04-01   to  2021-03-31

 Partnership

Take a look of project's partnership.

# participants  country  role  EC contrib. [€] 
1    IMPERIAL COLLEGE OF SCIENCE TECHNOLOGY AND MEDICINE UK (LONDON) coordinator 224˙933.00

Map

 Project objective

Cell therapy has emerged as a promising therapeutic strategy for cardiac repair, showing modest cardiomyocyte protection and infarct size reduction. It is under debate whether these outcomes are due to the implanted cells or their paracrine factors, as cells are scarce within a few weeks post-implantation. Regardless, this is still not sufficient to promote cardiac remuscularization and reverse medium to severe myocardium injury and fibrosis. Improved cell retention has been achieved with a substantial bulk of implanted cells, but highly associated to graft-induced arrhythmia, representing a significant challenge for clinical translation. The present study seeks to promote cardiac remuscularization after infarct, by improving the retention of cardiac cells and their paracrine factors without causing graft-induced arrhythmia. To do so, a conductive, self-doping and biodegradable oligoEDOT-heparin biomaterial will be synthesized and studied on in vitro and in vivo cardiac infarct models. The conductive EDOT oligomer moiety is envisaged to act as an electrical sink to shield the cardiac tissue from mismatched electromechanical impulses, while heparin will facilitate cardiac cell support and loading of regenerative factors, besides its recently documented doping capacity. The results of this fellowship are expected to overcome low cell retention and graft-induced arrhythmia, two of the biggest obstacles for translation in cardiac cell therapy, but also contribute with new insights regarding conductivity in materials and biological systems, to multiple fields of materials chemistry, medicine and bioelectronics. The world-class academic environment, collaborations and combined interdisciplinary expertise in biomaterials and cardiovascular sciences make the proposed fellowship activities ideally placed for enhancing my career prospects and consolidating my host and Europe in a leading position for translational research.

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