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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

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Fax: +49 (201) 723 - 5480
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Acute coronary syndromes represent one of the leading single causes of death worldwide. In patients with acute myocardial infarction, the treatment of choice is early and successful restoration of myocardial perfusion. The process of restoring blood flow to the ischemic myocardium, however, can induce injury itself. Emerging evidence points to a pivotal role for the first few minutes of reperfusion.

PD Dr. rer. nat. Hendgen-Cotta’s research interest includes mitochondria, which are central players in cell death by apoptotic, autophagic and programmed necrotic pathways during his early phase. This relates to the generation of toxic reactive oxygen species (ROS), deteriorated calcium signaling and perturbation of the mitochondrial integrity and function. In an in vivo ischemia/reperfusion (I/R) model she has discovered that myoglobin-mediated nitric oxide generation reduces complex I activity and ROS generation in the early phase of reperfusion. Now, she has focuses on defining events in cell death: mitochondrial outer membrane permeabilization or rupture, allowing cytochrome c and other apoptogens release, and disturbance of the inner mitochondrial membrane potential, precipitating mitochondrial dysfunction. Her work investigates changes in mitochondrial morphology, the formation of a protein/lipid pore in the mitochondrial outer membrane (MOMP) and oxidation of mitochondrial constituents, in particular the phospholipid cardiolipin, during the early phase of reperfusion.

Sonja Esfeld, M.Sc. is exploring the role of the BH3-only protein BNIP3 (Bcl-2 family members BCL2/adenovirus E1B 19 kDa protein-interacting protein 3) in I/R injury. In an in vivo I/R mouse model with 30 min of ischemia followed by 24 h reperfusion she has discovered that the inhibition of BNIP3 by blockade as well as genetic ablation leads to a significant reduction of the infarct size by 49%. Death signals ultimately converge on Bax, member of the Bcl-2 familiy, to promote MOMP. Prior studies provided hints that BNIP3 initiates the formation of MOMP. Her work investigates the molecular pathology of how BNIP3 dictates cardiomyocyte death by mediating pore formation and driving mitochondrial membrane depolarization by using the in vivo I/R model as well as isolated cardiomyocytes and mitochondria.

PD Dr. med. Matthias Totzeck research interest includes dysregulated calcium signaling in myocardial infarction, which is believed to be transferred into necrosis and apoptosis particularly by calpains. In I/R, calpains exhibit a deleterious activity particularly affecting mitochondria. This relates to a deterioration of mitochondrial respiratory chain and a crosstalk with key signal mediators of outer membrane permeabilization and fusion/fission by cleavage of the effector molecules and particularly affecting Bax. While calpain inhibition is generally possible, experimental studies have generated incongruent results. Induction of nitroso species formation from NO is largely capable of reducing myocardial I/R injury. Dr. Totzeck has demonstrated that a remote ischemic preconditioning approach is capable of generating a S-nitrosation switch. Short episodes of upper extremity I/R as performed with a blood pressure cuff lead to shear stress and hyperemia followed by increased circulating nitrite levels. After transport to the heart this can be translated into a protective signal, modifying mitochondrial complex one and reduce complex I activity in association with reduced ROS and I/R injury. S-nitrosation of calpains as seen in vitro may provide a targeted modification to protect the myocardium. Therefore, he intends to investigate the role of calpains in the early phase of reperfusion and whether the deleterious calpain activity can be inhibited by targeted posttranslational modification.

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