• E-mail :[email]
  • Phone : +33658268220
  • Location : Nice, France
Last update 2011-03-25 13:40:05.541

Kay-Dietrich Wagner MD, PhD

Course and current status

2007 – present: Group leader, INSERM AVENIR, INSERM U907, Directeur de Recherche INSERM 2005-2008: INSERM Young Investigator (CDD) 2003 – 2005: EMBO Long-term fellow, INSERM U636, Centre de Biochimie, Nice, France 02/2004: Postdoctoral lecture qualification in Physiology (Habilitation), Humboldt-University zu Berlin (Charité) 1998 - 2003: Post-doctoral research associate, Institute of Physiology, Humboldt-University zu Berlin (Charité) 1998 thesis: „Effects of hypoxia and reoxygenation on contractile function of human atrial trabeculae and rat papillary muscles – cardioprotective mechanisms“ (summa cum laude) 1996-1998: Resident, MD, Clinic for Cardiology, Angiology, and Pulmonology, Humboldt-University zu Berlin (Charité) 1995-1996: Junior Resident in Cardiology, Cardiac Surgery, Paediatrics, Gynaecology Humboldt-University zu Berlin (Charité) 1990-1996: Study of Medicine at the Humboldt-University zu Berlin (Charité)

Scientific summary

Chronic ischemic heart disease and myocardial infarction are the most common causes for morbidity and mortality. A survived myocardial infarction (MI) results in the long run in collateral formation and the development of cardiac hypertrophy. We could show that WT1 is essential for coronary vessel formation and it is stimulated by hypoxia, which is mediated via direct transcriptional activation by HIF-1. We identified the TrkB Neurotrophin-Receptor is a transcriptional target of WT1 in vascular development. Recently, we showed that WT1 is also critically involved in tumour angiogenesis via activation of the ETS-1 transcription factor and its down-stream target genes.

Our future research serves a two-fold purpose.  Firstly, we will address a possible use of WT1 and its downstream targets for novel approaches in directed cardiac angiogenesis in chronic ischemic heart disease.  Secondly, we plan to extend our knowledge about molecules involved in angiogenesis and to explore potential novel pharmacological approaches to induce angiogenesis in the heart. 

These experiments will give us not only insights into the role of WT1 in vasculogenesis and the possibility to identify novel molecules involved in vascular development, but also offer for the future potential approaches to modify the vascular response in the heart providing possibly new tools for the treatment of cardiac vascular disease.

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