E. Redox Regulation

Redox regulation: ischemia, hypoxia, and reactive oxygen species

Faculty involved

T.Acker, S. Bellusci, R.P. Brandes, T. Braun, B. Brüne, S. Dimmeler, W. Eberhardt, I. Fleming, G. Geisslinger, H.A. Ghofrani, W. Kummer, R.E. Morty, J. Pfeilschifter, M. Potente, S. Rohrbach, H. Sauer, K.D. Schlüter, R. Schulz, R.T. Schermuly, L. Schmitz, D. Steinhilber, N. Weissmann, K. Zacharowski, A.M. Zeiher

Subject

Alterations in cellular oxygen supply are key events in most cardio-pulmonary diseases. Ischemia, hypoxia and reoxygenation are all directly linked to changes in the cellular redox state and the generation of reactive oxygen species (ROS). Hypoxia, ROS and in a broader sense gaseous transmitters that alter the redox environment (H2S, CO, NO) also play an important role as signalling molecules, and specialised enzymes have been identified as sources of these redox mediators. In this area, the molecular mechanisms underlying redox-signalling will be identified, focussing on specific redox-mediated protein and lipid modifications to uncover novel targets that specifically interfere with cardio-pulmonary disease processes. The aim of this area is to shift the clinical approach away from symptomatic treatment with antioxidants towards a specific site directed inhibitory strategy, by utilising compounds that target individual generator and effector systems of redox-signalling. The concept of specific and compartmentalised redox-signalling will be tested in samples obtained from patients, animal and organ experiments as well as tissue culture. Site-specific probes to alter and analyse redox-signalling will be developed.

E. Redox Regulation

Redox regulation: ischemia, hypoxia, and reactive oxygen species

Research Area Leaders

Faculty involved

Subject