Research Scientist (m/f/d)

full-time – JobID: P0035V237

at the earliest possible date searched for the Institute of Experimental Cardiology (Internal Medicine 8).

Cardiovascular diseases are the leading cause of death in western countries and represent one of the major medical challenges of our time. The prevalence of acute and chronic heart failure with reduced as well as preserved ejection fraction (HFrEF and HFpEF) is currently increasing dramatically worldwide. The Institute for Experimental Cardiology is dedicated to investigate the molecular basis of various forms of cardiac diseases and is a central institute in the German Center for Cardiovascular Research (DZHK). Our institute is seeking for a highly motivated research scientist at the next possible time point. You will be responsible for the development, implementation and refinement of preclinical small animal models in including surgical techniques. As the coordinator of our resident small animal core you will provide your outstanding technical and scientific expertise to supervise and coordinate a team of well-trained specialized technicians.

Our institute has a long lasting experience in preclinical models of cardiovascular diseases. We have applied various genetic, pharmacological and surgical small animal models to identify and study key signaling pathways that are causative for heart diseases (see 1-5). Our small animal core is and will be equipped with all modern state-of-the-art technologies for comprehensive cardiovascular preclinical in vivo research (e.g. mouse microsurgery platforms, VisualSonics Vevo Echocardiography, DSI PhysioTel Telemetry, MR Solutions PET/MRI is planned).

Important publications of our research work you can find here:

1. Jebessa, Z. H. et al. The lipid droplet-associated protein ABHD5 protects the heart through proteolysis of HDAC4. Nature metabolism 1, 1157-1167, doi:10.1038/s42255-019-0138-4 (2019).

2. Lehmann, L. H. et al. A proteolytic fragment of histone deacetylase 4 protects the heart from failure by regulating the hexosamine biosynthetic pathway. Nature medicine 24, 62-72, doi:10.1038/nm.4452 (2018).

3. Kronlage, M. et al. O-GlcNAcylation of Histone Deacetylase 4 Protects the Diabetic Heart From Failure. Circulation 140, 580-594, doi:10.1161/CIRCULATIONAHA.117.031942 (2019).

4. Weinreuter, M. et al. CaM Kinase II mediates maladaptive post-infarct remodeling and pro-inflammatory chemoattractant signaling but not acute myocardial ischemia/reperfusion injury. EMBO molecular medicine 6, 1231-1245, doi:10.15252/emmm.201403848 (2014).

5. Kreusser, M. M. et al. Cardiac CaM Kinase II genes delta and gamma contribute to adverse remodeling but redundantly inhibit calcineurin-induced myocardial hypertrophy. Circulation 130, 1262-1273, doi:10.1161/CIRCULATIONAHA.114.006185 (2014).