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Boengler K, Bencsik P, Palóczi J, et al. Lack of Contribution of p66shc and Its Mitochondrial Translocation to Ischemia-Reperfusion Injury and Cardioprotection by Ischemic Preconditioning. Front Physiol. 2017;8:733doi: 10.3389/fphys.2017.00733.
Boengler, K., Bencsik, P., Palóczi, J., Kiss, K., Pipicz, M., Pipis, J., Ferdinandy, P., Schlüter, K. D., & Schulz, R. (2017). Lack of Contribution of p66shc and Its Mitochondrial Translocation to Ischemia-Reperfusion Injury and Cardioprotection by Ischemic Preconditioning. Frontiers in physiology, 8733. https://doi.org/10.3389/fphys.2017.00733
Boengler, Kerstin, et al. "Lack of Contribution of p66shc and Its Mitochondrial Translocation to Ischemia-Reperfusion Injury and Cardioprotection by Ischemic Preconditioning." Frontiers in physiology vol. 8 (2017): 733. doi: https://doi.org/10.3389/fphys.2017.00733
Boengler K, Bencsik P, Palóczi J, Kiss K, Pipicz M, Pipis J, Ferdinandy P, Schlüter KD, Schulz R. Lack of Contribution of p66shc and Its Mitochondrial Translocation to Ischemia-Reperfusion Injury and Cardioprotection by Ischemic Preconditioning. Front Physiol. 2017 Oct 05;8:733. doi: 10.3389/fphys.2017.00733. eCollection 2017. PMID: 29051737; PMCID: PMC5633811.
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Front Physiol. 2017 Oct 05;8:733. doi: 10.3389/fphys.2017.00733. eCollection 2017.

Lack of Contribution of p66shc and Its Mitochondrial Translocation to Ischemia-Reperfusion Injury and Cardioprotection by Ischemic Preconditioning.

Frontiers in physiology

Kerstin Boengler, Péter Bencsik, János Palóczi, Krisztina Kiss, Márton Pipicz, Judit Pipis, Péter Ferdinandy, Klaus-Dieter Schlüter, Rainer Schulz

Affiliations

  1. Physiologisches Institut, Justus-Liebig-Universität, Giessen, Germany.
  2. Pharmahungary Group, Szeged, Hungary.
  3. Cardiovascular Research Group, Department of Biochemistry, University of Szeged, Szeged, Hungary.
  4. Department of Pharmacology and Pharmacotherapy, Semmelweis University, Budapest, Hungary.

PMID: 29051737 PMCID: PMC5633811 DOI: 10.3389/fphys.2017.00733

Abstract

Whereas high amounts of reactive oxygen species (ROS) contribute to cardiac damage following ischemia and reperfusion (IR), low amounts function as trigger molecules in the cardioprotection by ischemic preconditioning (IPC). The mitochondrial translocation and contribution of the hydrogen peroxide-generating protein p66shc in the cardioprotection by IPC is unclear yet. In the present study, we investigated the mitochondrial translocation of p66shc, addressed the impact of p66shc on ROS formation after IR, and characterized the role of p66shc in IR injury

Keywords: ischemia/reperfusion; ischemic preconditioning; mitochondria; p66shc; reactive oxygen species

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