Forschergruppe 923 CARVAS

Molecular Dissection of Cardiovascular Function
Prof. Dr. med. Franz Hofmann
Sprecher
Prof. Dr. med. Karl-Ludwig Laugwitz
stellvertretender Sprecher
Sekretariat:
TU München
Stefanie Strasser
Institut für Pharmakologie und Toxikologie
TU München,
Biedersteiner Str. 29
80802 München
Tel: 089-4140-3240/41
Fax: 089-4140-3250
e-mail: strasser(at)lrz.tum.de


Funding period: August 2007 – July 2010
Concept of the Forschergruppe
Cardiovascular diseases are the leading cause of death in Europe. However, surprisingly little information is available about the mechanisms and signalling cascades necessary to maintain the cardiovascular system in a non-disease state. The assorted flow of information within cellular pathways largely relies on reversible and specific protein interactions.
Therefore, targeting intracellular signalling pathways is an especially demanding task, requiring research at the interface of molecular biology, physiology and live cell imaging. To accomplish this goal, molecular interactions of signalling molecules will be characterised functionally and structurally in specific cell types in vitro and in gene-targeted mice in vivo within the framework of the proposed research unit (FG). The FG integrates groups that have worked intensely on molecular switches that regulate cardiovascular functions.
The advantages of the proposed FG is that each group provides different expertise that is needed by other groups and the interdisciplinary approach of researchers working on basic and disease-related themes of cardiovascular sciences. Our major goal is to dissect signalling pathways that govern cardiac cell-fate decisions of myocytes, endothelial and smooth muscle cells, that control the rhythm of the heart (sinus node), that prevent cardiac hypertrophy, and that regulate vascular functions in health and disease.
Similar or identical signal cascades are investigated to provide the necessary information for different functions in each subtopic. Aims of the research activities are (i) to determine the functional contribution(s) of specific signalling pathways in cardiovascular physiology and (ii) to identify molecular “hot spots” in disease states for novel treatment options.
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