LSHM-CT-2005-018833

Coordinator: Gerd Hasenfuss
Team Leader: Alexandra Zahradníková

Duration: January 2006 – December 2010
Coordinating Organization: University of Gottingen, Germany

Annotation:

The project is aimed on genomics of the signalling mechanisms that play a role in heart failure, a disease very frequent in European population. The ultimate objective is to develop more effective treatment of this syndrome. Therefore the consortium involves laboratories and institutions that specialize in basic, pharmaceutical and clinical research, as well as SMEs. The project is based on the hypothesis that the changes in the structure and function of the heart that precede heart failure can be divided into beneficial (that improve cardiac function) and maladaptive (that lead to heart failure), and that it is possible to selectively inhibit maladaptive changes. The differences between subjects different in the predisposition to heart failure will be analyzed, genomic and proteomic screening performed, and the findings will be translated into pharmacological and clinical practice. The project has an important educational and training component (conferences, workshops).

Keywords:

Heart failure, hypertrophic signalling, cardiac myocyte

Objectives:

The goal of the EUGeneHeart project is the development of new approaches to prevent and treat heart failure through analysis of the genomics of signalling. The strategy is based on the hypothesis that beneficial as well as maladaptive forms of hypertrophy exist and that heart failure is frequently preceded by maladaptive hypertrophy. We will dissect both adaptive and maladaptive signalling in hypertrophy to identify beneficial and maladaptive components of signal transduction in hypertrophy and heart failure. (see http://www.eugeneheart.eu/38.htm)

The team at the Department of Muscle Cell Research IMPG SAS will participate in determining, how and why is the ability of the heart to contract in response to electrical stimuli changed, and how are these changes affected by changes in gene expression and by drugs.

Publications: