PortalPublikationenReversal of Mitochondrial Transhydrogenase Causes Oxidative ...

Reversal of Mitochondrial Transhydrogenase Causes Oxidative Stress in Heart Failure

Standard

Reversal of Mitochondrial Transhydrogenase Causes Oxidative Stress in Heart Failure. / Nickel, Alexander G; von Hardenberg, Albrecht; Hohl, Mathias; Löffler, Joachim R; Kohlhaas, Michael; Becker, Janne; Reil, Jan-Christian; Kazakov, Andrey; Bonnekoh, Julia; Stadelmaier, Moritz; Puhl, Sarah-Lena; Wagner, Michael; Bogeski, Ivan; Cortassa, Sonia; Kappl, Reinhard; Pasieka, Bastian; Lafontaine, Michael; Lancaster, C Roy D; Blacker, Thomas S; Hall, Andrew R; Duchen, Michael R; Kästner, Lars; Lipp, Peter; Zeller, Tanja; Müller, Christian; Knopp, Andreas; Laufs, Ulrich; Böhm, Michael; Hoth, Markus; Maack, Christoph.

in: CELL METAB, Jahrgang 22, Nr. 3, 01.09.2015, S. 472-484.

Publikationen: SCORING: Beitrag in Fachzeitschrift/Zeitung › SCORING: Zeitschriftenaufsatz › Forschung › Begutachtung

Harvard

Nickel, AG, von Hardenberg, A, Hohl, M, Löffler, JR, Kohlhaas, M, Becker, J, Reil, J-C, Kazakov, A, Bonnekoh, J, Stadelmaier, M, Puhl, S-L, Wagner, M, Bogeski, I, Cortassa, S, Kappl, R, Pasieka, B, Lafontaine, M, Lancaster, CRD, Blacker, TS, Hall, AR, Duchen, MR, Kästner, L, Lipp, P, Zeller, T, Müller, C, Knopp, A, Laufs, U, Böhm, M, Hoth, M & Maack, C 2015, 'Reversal of Mitochondrial Transhydrogenase Causes Oxidative Stress in Heart Failure', CELL METAB, Jg. 22, Nr. 3, S. 472-484. https://doi.org/10.1016/j.cmet.2015.07.008

APA

Nickel, A. G., von Hardenberg, A., Hohl, M., Löffler, J. R., Kohlhaas, M., Becker, J., Reil, J-C., Kazakov, A., Bonnekoh, J., Stadelmaier, M., Puhl, S-L., Wagner, M., Bogeski, I., Cortassa, S., Kappl, R., Pasieka, B., Lafontaine, M., Lancaster, C. R. D., Blacker, T. S., ... Maack, C. (2015). Reversal of Mitochondrial Transhydrogenase Causes Oxidative Stress in Heart Failure. CELL METAB, 22(3), 472-484. https://doi.org/10.1016/j.cmet.2015.07.008

Vancouver

Nickel AG, von Hardenberg A, Hohl M, Löffler JR, Kohlhaas M, Becker J et al. Reversal of Mitochondrial Transhydrogenase Causes Oxidative Stress in Heart Failure. CELL METAB. 2015 Sep 1;22(3):472-484. https://doi.org/10.1016/j.cmet.2015.07.008

Bibtex

@article{2a27e943baaa429f9a8c21c70ed97dcf,
title = "Reversal of Mitochondrial Transhydrogenase Causes Oxidative Stress in Heart Failure",
abstract = "Mitochondrial reactive oxygen species (ROS) play a central role in most aging-related diseases. ROS are produced at the respiratory chain that demands NADH for electron transport and are eliminated by enzymes that require NADPH. The nicotinamide nucleotide transhydrogenase (Nnt) is considered a key antioxidative enzyme based on its ability to regenerate NADPH from NADH. Here, we show that pathological metabolic demand reverses the direction of the Nnt, consuming NADPH to support NADH and ATP production, but at the cost of NADPH-linked antioxidative capacity. In heart, reverse-mode Nnt is the dominant source for ROS during pressure overload. Due to a mutation of the Nnt gene, the inbred mouse strain C57BL/6J is protected from oxidative stress, heart failure, and death, making its use in cardiovascular research problematic. Targeting Nnt-mediated ROS with the tetrapeptide SS-31 rescued mortality in pressure overload-induced heart failure and could therefore have therapeutic potential in patients with this syndrome.",
keywords = "Adenosine Triphosphate/metabolism, Animals, Cells, Cultured, Glutathione/metabolism, Heart Failure/metabolism, Mice, Inbred C57BL, Mitochondria, Heart/metabolism, NADP/metabolism, NADP Transhydrogenases/metabolism, Oxidative Stress, Reactive Oxygen Species/metabolism",
author = "Nickel, {Alexander G} and {von Hardenberg}, Albrecht and Mathias Hohl and L{\"o}ffler, {Joachim R} and Michael Kohlhaas and Janne Becker and Jan-Christian Reil and Andrey Kazakov and Julia Bonnekoh and Moritz Stadelmaier and Sarah-Lena Puhl and Michael Wagner and Ivan Bogeski and Sonia Cortassa and Reinhard Kappl and Bastian Pasieka and Michael Lafontaine and Lancaster, {C Roy D} and Blacker, {Thomas S} and Hall, {Andrew R} and Duchen, {Michael R} and Lars K{\"a}stner and Peter Lipp and Tanja Zeller and Christian M{\"u}ller and Andreas Knopp and Ulrich Laufs and Michael B{\"o}hm and Markus Hoth and Christoph Maack",
note = "Copyright {\textcopyright} 2015 Elsevier Inc. All rights reserved.",
year = "2015",
month = sep,
day = "1",
doi = "10.1016/j.cmet.2015.07.008",
language = "English",
volume = "22",
pages = "472--484",
journal = "CELL METAB",
issn = "1550-4131",
publisher = "Cell Press",
number = "3",

}

RIS

TY - JOUR

T1 - Reversal of Mitochondrial Transhydrogenase Causes Oxidative Stress in Heart Failure

AU - Nickel, Alexander G

AU - von Hardenberg, Albrecht

AU - Hohl, Mathias

AU - Löffler, Joachim R

AU - Kohlhaas, Michael

AU - Becker, Janne

AU - Reil, Jan-Christian

AU - Kazakov, Andrey

AU - Bonnekoh, Julia

AU - Stadelmaier, Moritz

AU - Puhl, Sarah-Lena

AU - Wagner, Michael

AU - Bogeski, Ivan

AU - Cortassa, Sonia

AU - Kappl, Reinhard

AU - Pasieka, Bastian

AU - Lafontaine, Michael

AU - Lancaster, C Roy D

AU - Blacker, Thomas S

AU - Hall, Andrew R

AU - Duchen, Michael R

AU - Kästner, Lars

AU - Lipp, Peter

AU - Zeller, Tanja

AU - Müller, Christian

AU - Knopp, Andreas

AU - Laufs, Ulrich

AU - Böhm, Michael

AU - Hoth, Markus

AU - Maack, Christoph

N1 - Copyright © 2015 Elsevier Inc. All rights reserved.

PY - 2015/9/1

Y1 - 2015/9/1

N2 - Mitochondrial reactive oxygen species (ROS) play a central role in most aging-related diseases. ROS are produced at the respiratory chain that demands NADH for electron transport and are eliminated by enzymes that require NADPH. The nicotinamide nucleotide transhydrogenase (Nnt) is considered a key antioxidative enzyme based on its ability to regenerate NADPH from NADH. Here, we show that pathological metabolic demand reverses the direction of the Nnt, consuming NADPH to support NADH and ATP production, but at the cost of NADPH-linked antioxidative capacity. In heart, reverse-mode Nnt is the dominant source for ROS during pressure overload. Due to a mutation of the Nnt gene, the inbred mouse strain C57BL/6J is protected from oxidative stress, heart failure, and death, making its use in cardiovascular research problematic. Targeting Nnt-mediated ROS with the tetrapeptide SS-31 rescued mortality in pressure overload-induced heart failure and could therefore have therapeutic potential in patients with this syndrome.

AB - Mitochondrial reactive oxygen species (ROS) play a central role in most aging-related diseases. ROS are produced at the respiratory chain that demands NADH for electron transport and are eliminated by enzymes that require NADPH. The nicotinamide nucleotide transhydrogenase (Nnt) is considered a key antioxidative enzyme based on its ability to regenerate NADPH from NADH. Here, we show that pathological metabolic demand reverses the direction of the Nnt, consuming NADPH to support NADH and ATP production, but at the cost of NADPH-linked antioxidative capacity. In heart, reverse-mode Nnt is the dominant source for ROS during pressure overload. Due to a mutation of the Nnt gene, the inbred mouse strain C57BL/6J is protected from oxidative stress, heart failure, and death, making its use in cardiovascular research problematic. Targeting Nnt-mediated ROS with the tetrapeptide SS-31 rescued mortality in pressure overload-induced heart failure and could therefore have therapeutic potential in patients with this syndrome.

KW - Adenosine Triphosphate/metabolism

KW - Animals

KW - Cells, Cultured

KW - Glutathione/metabolism

KW - Heart Failure/metabolism

KW - Mice, Inbred C57BL

KW - Mitochondria, Heart/metabolism

KW - NADP/metabolism

KW - NADP Transhydrogenases/metabolism

KW - Oxidative Stress

KW - Reactive Oxygen Species/metabolism

U2 - 10.1016/j.cmet.2015.07.008

DO - 10.1016/j.cmet.2015.07.008

M3 - SCORING: Journal article

C2 - 26256392

VL - 22

SP - 472

EP - 484

JO - CELL METAB

JF - CELL METAB

SN - 1550-4131

IS - 3

ER -