Abstract
Mitochondria are the main source for ATP, but also reactive oxygen species (ROS). While NADH is required for ATP production, NADPH regenerates anti-oxidative capacity to prevent excessive ROS emission. The mitochondrial transhydrogenase links NADH with NADPH pools and is mutated in C57BL/6 mice from Jackson Laboratories. While in most scenarios, the transhydrogenase regenerates NADPH in the forward mode, it can reverse under pathological conditions and cause oxidative stress and heart failure.
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Albrecht von Hardenberg 2006–2013 Medizinstudium an den Universitäten Homburg und Oviedo, Spanien. 2009–2016 Promotion in der Arbeitsgruppe von C. Maack. Seit 2013 Assistenzarzt in der Klinik für Innere Medizin III, Universitätsklinikum des Saarlandes, Homburg.
Christoph Maack 1993–2000 Medizinstudium an der Universität zu Köln. 2000–2002 und 2005–2012 Assistenzarzt an der Klinik für Innere Medizin III, Universitätsklinikum des Saarlandes, Homburg, seit 2012 dort Oberarzt. 2002–2005 Postd°C an der Johns Hopkins University in Baltimore, MD, USA in der Arbeitsgruppe von Prof. Dr. B. O’Rourke. 2006–2011 Emmy Noether-Programm, seit 2012 Heisenberg-Professur für Kardiovaskuläre Physiologie und Bioenergetik.
Alexander Nickel 1998–2004 Ökotrophologiestudium an der TU München. 2004–2009 Promotion im Bereich Nierenphysiologie. Seit 2009 wissenschaftlicher Mitarbeiter in der Arbeitsgruppe von C. Maack, Klinik für Innere Medizin III, Universitätsklinikum des Saarlandes, Homburg.
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Von Hardenberg, A., Nickel, A. & Maack, C. Mitochondriale Transhydrogenase: Yin und Yang der antioxidativen Kapazität. Biospektrum 23, 22–24 (2017). https://doi.org/10.1007/s12268-017-0760-1
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DOI: https://doi.org/10.1007/s12268-017-0760-1