ENSIG-MIRNA

Endocannabinoid signaling in heart failure: functional relevance of microRNAs

 Coordinatore MEDIZINISCHE HOCHSCHULE HANNOVER 

 Organization address address: Carl-Neuberg-Strasse 1
city: HANNOVER
postcode: 30625

contact info
Titolo: Mr.
Nome: Frank
Cognome: Dittrich
Email: send email
Telefono: 495115000000

 Nazionalità Coordinatore Germany [DE]
 Totale costo 75˙000 €
 EC contributo 75˙000 €
 Programma FP7-PEOPLE
Specific programme "People" implementing the Seventh Framework Programme of the European Community for research, technological development and demonstration activities (2007 to 2013)
 Code Call FP7-PEOPLE-2011-CIG
 Funding Scheme MC-CIG
 Anno di inizio 2011
 Periodo (anno-mese-giorno) 2011-08-01   -   2014-07-31

 Partecipanti

# participant  country  role  EC contrib. [€] 
1    MEDIZINISCHE HOCHSCHULE HANNOVER

 Organization address address: Carl-Neuberg-Strasse 1
city: HANNOVER
postcode: 30625

contact info
Titolo: Mr.
Nome: Frank
Cognome: Dittrich
Email: send email
Telefono: 495115000000

DE (HANNOVER) coordinator 75˙000.00

Mappa


 Word cloud

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tissue    gene    cardiac    pro    sensitive    explore    heart    endocannabinoid    regulated    microrna    signaling    therapeutic    injury    expression    micrornas   

 Obiettivo del progetto (Objective)

'Heart failure is a primary cause of cardiovascular morbidity and mortality with raising economic burden. There is an increasing need for innovative novel therapies. MicroRNAs are novel regulators of gene expression and are implicated in cardiac development and pathologies including heart failure. Research is underway to explore the potential of microRNA-based therapeutics. However many basic research and clinical questions remain to be solved. Dysregulation of endocannabinoid signaling has been recently described in various diseases, including heart failure. Tissue injury induces increase of endocannabinoids which, in turn is pro-apoptotic, pro-fibrogenic, promote oxidati stress and cell death. Inhibitors of the cannabinoid CB1 receptor has been proven to be vasculo- and cardioprotective. Given that microRNAs can regulate global gene networks at the translational level, it is plausible that changes in the level of bioactive molecules, such as endocannabinoid in the failing heart are associated with altered activity of specific sets of microRNA-targets. To date, the effect of endogenous or pharmacological modulators of the endocannabinoid system on cardiac microRNA expression and the potential therapeutic consequences have not been explored. The overall goals of this proposal are 1) to determine the contribution of tissue injury induced endocannabinoid activation on the cardiac microRNA expression profile that is associated with the development of heart failure, 2) to identify functionally relevant microRNAs that are sensitive to the modulation of endocannabinoid signaling and 3) to explore the therapeutic potential of the identified endocannabinoid-regulated microRNAs in heart failure development. The proposed experiments will elucidate how endocannabinoid signaling alters sets of cardiac disease-regulated microRNAs and identify endocannabinoid-sensitive miRNAs relevant for future development of microRNA-based therapeutic approaches in the treatment of heart failure'

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