Reference : ROS-induced regulation of mitophagy and its failure in Parkinson’s disease
Scientific congresses, symposiums and conference proceedings : Poster
Life sciences : Biochemistry, biophysics & molecular biology
Computational Sciences
http://hdl.handle.net/10993/6936
ROS-induced regulation of mitophagy and its failure in Parkinson’s disease
English
Kolodkin, Alexey mailto [University of Luxembourg > Luxembourg Centre for Systems Biomedicine (LCSB) > >]
Ignatenko, Andrew mailto [University of Luxembourg > Faculty of Science, Technology and Communication (FSTC) > Engineering Research Unit >]
Simeonidis, Vangelis mailto [University of Luxembourg > Luxembourg Centre for Systems Biomedicine (LCSB) > >]
Sangar, Vineet [Institute for Systems Biology - ISB]
Choe, Charley [German Cancer Research Center]
Peters, Bernhard mailto [University of Luxembourg > Faculty of Science, Technology and Communication (FSTC) > Engineering Research Unit >]
Price, Nathan [Institute for Systems Biology - ISB]
Balling, Rudi mailto [University of Luxembourg > Luxembourg Centre for Systems Biomedicine (LCSB) > >]
Brady, Nathan [German Cancer Research Center]
May-2013
No
Mitochondria: from Signaling to Disease
May 5 - 7, 2013
Lisbon
Portugal
[en] ROS generation ; Parkinson's disease
[en] Reactive Oxygen Species (ROS) generation is an unavoidable background process in the normal functioning of the cell. The greatest contributor to ROS production is the electron transport chain (ETC) where O2 is reduced to H2O. Some incompletely-reduced oxygen species escape and oxidize a variety of organic molecules (e.g. proteins and lipids in the mitochondrial membrane), leading to molecular dysfunction and initiating a positive feedback loop leading to generation of even more active radicals. Increased ROS concentration damages mitochondria and further increases ROS generation. Healthy cells manage ROS enzymatically with superoxide dismutase and other enzymes, various antioxidants, and ultimately through increased mitophagy of damaged mitochondria. The precise tuning of the latter mechanism is crucial for cell survival and is controlled in the cell by a ROS-induced regulatory network, which consists of many components such as Nrf2, Keap1, Parkin and p62 with a rather complicated cross-talk (Figure 1). In many diseases (cancer, Parkinson’s disease (PD), Huntington’s disease (HD), etc.), various components of the ROS management network are altered. Deconstructing the molecular mechanisms underlying or resulting from these alterations might contribute to better understanding of the dynamics of related pathophysiological processes. We have built a kinetics-based model which recapitulates the consensus understanding of the mechanism responsible for cellular ROS – managing system.
http://hdl.handle.net/10993/6936

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