Klaassen Lab

First, we clinically and genetically characterize different cardiomyopathy cohorts to identify novel disease genes, to understand the mechanisms for heart failure, and to improve prognosis. Second, we investigate the specific role of the transcriptional regulator PRDM16 for cardiomyocyte development, cardiac function, and cardiomyopathy. Third, we aim to assess how Bcl-2-associated athanogene 3 (BAG3) and the heat shock protein 70 (HSP70) complex affect cardiomyocyte proteostasis as a potential target for heart failure therapy.

Our concept bundles excellence in pediatric as well as adult cardiology, molecular mechanisms of inherited cardiac diseases, and therapeutic approaches in cardiomyopathy.

As a pediatric cardiogenetics group we focus on the molecular genetics of cardiomyopathies,  arrhythmias, and structural congenital heart defects. Considerable progress in identifying the genes and pathways involved in left ventricular noncompaction cardiomyopathy (LVNC) has been made and this entity will continue be one main topic of our future research. Among the various projects and activities in the past 3 years at the ECRC the main progress has been made in identifying that mutation of the PRDM16 gene causes cardiomyopathy.

A short overview on our projects is shown in the corresponding sections.

Risk stratification in pediatric cardiomyopathies (RIKADA)

 

As part of the DZHK initiative (Deutsches Zentrum für Herz-Kreislauf-Forschung) the Pediatric Cardiology Department, DHZB (German Heart Centre Berlin), Director Prof. F. Berger, Berlin, participates for the partner-site Berlin. The general aim of the project is to characterize „Mechanisms of heart failure in congenital heart disease“. Genetic, molecular and imaging modalities are applied to identify predictors of adverse outcome.

Please contact us for further information.