Detailseite
Modulation of myocardial remodeling by Wnt-signaling
Antragsteller
Professor Dr. Stefan Hardt
Fachliche Zuordnung
Zellbiologie
Förderung
Förderung von 2009 bis 2015
Projektkennung
Deutsche Forschungsgemeinschaft (DFG) - Projektnummer 58160712
One of the essential factors for the improvement of prognosis after myocardial infarction is inhibition of adverse left ventricular remodeling (myocardial fibrosis, myocyte hypertrophy, left ventricular dilatation). Currently, there are no specific therapeutic strategies to prevent this process. The Wnt-pathway is an evolutionary conserved signaling mechanism, which regulates cardiogenesis. However, members of the Wnt-pathway are also expressed in the adult heart and there is accumulating evidence from the literature suggesting a crucial role in the myocardial remodeling process. Glycogen synthase kinase-3 (GSK-3), a negative regulator of cell growth, inhibits Wnt signaling and appears to be centrally involved in myocardial remodeling. Based on the current state of the literature, our previous work and preliminary data we propose to investigate the role of Wnt signaling in transgenic mouse models and cultured cardiac myocytes as for its role in myocardial function and myocardial remodeling following pathologic stress.
DFG-Verfahren
Forschungsgruppen