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B06 - The role of programmed cell death in mitochondrial hepatopathy

Hamid Kashkar
CECAD Research Center/Institute for Medical Microbiology, Immunology and Hygiene (IMMIH), University Hospital Cologne

E-mail: H.Kashkar(at)uni-koeln.de
Phone: +49 - 221 / 478 84091
For more information and contact please visit the KASHKAR LAB.

Abstract
Mitochondrial dysfunction result in tissue degeneration; frequently associated with elevated apoptosis within the affected tissues. However, whether and how apoptosis interferes with disease pathogenesis is still not determined. The central objective of this project is to mechanistically determine the role of apoptosis in tissue damage upon mitochondrial dysfunction by employing a model for mitochondrial hepatopathy. This knowledge will expand our view about the pathophysiology of mitochondrial diseases and will drive the development of therapeutically relevant agents that interfere with the dynamic interconnection between cell death and mitochondrial dysfunction.

Latest publication
Schüll, S., Günther, S.D., Brodesser, S., Seeger, J.M., Tosetti, B., Wiegmann, K., Pongratz, C., Diaz, F., Witt, A., Andree, M., Brinkmann, K., Krönke, M., Wiesner, R.J., and Kashkar, H. (2015). Cytochrome c oxidase deficiency accelerates mitochondrial apoptosis by activating ceramide synthase 6. Cell Death Dis. 6, e1691.