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Das Westdeutsche Herz- und Gefäßzentrum Essen mit der Klinik für Kardiologie und Angiologie befindet sich auf dem Gelände des Universitätsklinikums Essen. Sollten Sie die Routenplanung selbst vornehmen wollen, dann schauen Sie unsere Wegbeschreibung oder benutzen Sie bitte folgende Postadresse:

Hufelandstr. 55 | 45122 Essen

Bleiben sie mit uns in Kontakt

Fax: +49 (201) 723 - 5480
Lageplan des Klinikums

Standort

E-Mail: sonja.esfeld@uk-essen.de
Office: MFZ 3. OG Room 03.026
Telefon: +49 201 723 6011
Fax: +49 201 723 6973
Dr. rer. nat. Sonja Esfeld

BIO

Sonja Esfeld received her M.Sc. in 2011 from the Ruhr University Bochum in Biochemistry with the specialization in Molecular Medicine. She performed her master thesis at the West German Cancer Center at the University Hospital Essen. In 2012 she started her PhD program at the Heinrich-Heinrich University Düsseldorf Graduate School VIVID under the mentorship of Prof. Rassaf. In August 2015, she joined the University Hospital Essen as a member of the CardioScienceLabs at the Department of Cardiology and completed her PhD thesis in March 2016. Currently she is working as a postdoctoral researcher in our team.

RESEARCH INTERESTS

Mitochondria are ubiquitous organelles, playing a vital role in bioenergetics, metabolite biosynthesis and overall cellular homeostasis. Their functional activity needs to be tightly regulated, as evidenced by the growing number of pathologies in which mitochondrial dysfunction is either a causative or compounding factor. During the early phase of reperfusion after myocardial infarction mitochondria are central players in cell death. The permeabilization of the mitochondrial outer membrane (MOM) is a major determinant of apoptosis and necrosis. Previous studies demonstrated that Bcl-2 family members are involved in the formation of the MOM pore (MOMP) that leads to loss of apoptogens, caspase activation and cell death. The underlying mechanism is still unidentified.
My work focuses on the role of Bcl-2 family member BNIP3 during the early phase of reperfusion following myocardial ischemia in an in vivo mouse model with reversible left coronary artery occlusion. The objective target is to find the underlying mechanisms for cell death orchestrated by BNIP3 and to search for novel therapeutic targets for the treatment of myocardial I/R injury.

Abstracts

  1. Ecken S, Korste-Wieberneit F, Kelm M, Hendgen-Cotta U, Rassaf T. (2015)  – Bnip3 drives mitochondrial damage in the early phase of myocardial ischemia/reperfusion injury. Clin Res Cardiol. 104, Suppl 1, P721, DGK Mannheim
  2. Ecken S, Hendgen-Cotta U, Kelm M, Rassaf T. (2014) – Bnip3 is associated with Bax activation during myocardial ischemia/reperfusion injury in vivo. Eur Heart J. 35 Suppl 1,  ESC Congress Barcelona
  3. Ecken S, Hendgen-Cotta U, Kelm M, Rassaf (2014) Bnip3 is associated with cell death during myocardial ischemia/reperfusion injury in vivo DGK Mannheim

Oral Presentations

  • 08/15 – ESC Congress London, Rapid Fire Abstract; Bnip3 drives mitochondrial damage in the early phase of myocardial ischemia/reperfusion. Eur Heart J. 36 Suppl 1
  • 07/15 – Vivid-Retreat Wermelskirchen; The role of BNIP3 in myocardial ischemia/reperfusion injury.
  • 07/14 – Advanced Training, University Hospital Düsseldorf; Bnip3 is associated with Bax activation during myocardial ischemia/reperfusion injury in vivo.
  • 06/14 – Vivid-Retreat Wermelskirchen; The role of BNIP3 in myocardial ischemia/reperfusion injury.
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