CARDIOPREVENT

INTEGRATION OF GENOMICS AND CARDIOMETABOLIC PLASMA BIOMARKERS FOR IMPROVED PREDICTION AND PRIMARY PREVENTION OF CARDIOVASCULAR DISEASE

Coordinatore	LUNDS UNIVERSITET    more Spiacenti, non ci sono informazioni su questo coordinatore. Contattare Fabio per maggiori infomrazioni, grazie.
Nazionalità Coordinatore	Sweden [SE]
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	2011
Periodo (anno-mese-giorno)	2011-12-01   -   2016-11-30

 Partecipanti

#	participant	country	role	EC contrib. [€]
1	INSTITUT NATIONAL DE LA SANTE ET DE LA RECHERCHE MEDICALE (INSERM)  Organization address address: 101 Rue de Tolbiac city: PARIS postcode: 75654 contact info Titolo: Dr. Nome: Sylviane Cognome: Inocencio Email: send email Telefono: +33 1 480 73 391 Fax: +33 1 480 73 432	FR (PARIS)	beneficiary	150˙000.00
2	LUNDS UNIVERSITET  Organization address address: Paradisgatan 5c city: LUND postcode: 22100 contact info Titolo: Prof. Nome: Lennart Cognome: Råstam Email: send email Telefono: 4640391377 Fax: 4640391370	SE (LUND)	hostInstitution	1˙350˙000.00
3	LUNDS UNIVERSITET  Organization address address: Paradisgatan 5c city: LUND postcode: 22100 contact info Titolo: Prof. Nome: Olle Sten Cognome: Melander Email: send email Telefono: 4640391209 Fax: 460391222	SE (LUND)	hostInstitution	1˙350˙000.00

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 Obiettivo del progetto (Objective)

'By taking advantage of great experience in genetic and cardiovascular epidemiology and some of the largest cohorts in the world including 60 000 unique individuals, the applicant aims at (1) improving CVD risk prediction and (2) identifying mechanisms causally related to CVD development in order to provide novel targets for drug discovery and targeted life style interventions for use in primary prevention. In SUBPROJECT 1 we aim at identifying disease causing alleles of loci implicated in CVD by Genome Wide Association Studies (GWAS) and to identify rare alleles with large impact on human CVD. We thus perform whole exome and targeted sequencing in early CVD cases and healthy controls and evaluate all identified variants by relating them to incident CVD in 60.000 individuals. Further, we will create a score of all validated CVD gene variants and test whether such a score improves clinical risk assessment over and above traditional risk factors. In SUBPROJECT 2 we test whether the plasma metabolome- a phenotype representing the product of dietary intake and inherent (e.g. genetic) metabolism- differs between incident CVD cases and controls and between individuals with high and low CVD genetic risk. We further test whether a life style intervention differentially alters the plasma metabolome between individuals with high and low CVD genetic risk. Finally, we will elucidate the mechanisms underlying CVD genetic associations by testing whether myocardial expression of such genes are affected by experimental myocardial infarction (MI) and whether heart function, MI size and the plasma metabolome are affected by adenoviral myocardial CVD gene transfer in rats. In SUBPROJECT 3 we test whether glucose metabolism and CVD risk factors can be ameliorated by suppressing vasopressin (VP) by increased water intake in humans. Finally, we test which of the 3 VP receptors is responsible for adverse glucometabolic VP effects in rats by specific VP receptor pharmacological studies.'