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Endonuclease G is a novel determinant of cardiac hypertrophy and mitochondrial function

Author

Listed:
  • Chris McDermott-Roe

    (Medical Research Council Clinical Sciences Centre, Faculty of Medicine, Imperial College London, Hammersmith Hospital)

  • Junmei Ye

    (Cell Signaling & Apoptosis Group, University Lleida, Biomedical Research Institute of Lleida (IRBLLEIDA), Avenida Rovira Roure 80)

  • Rizwan Ahmed

    (Medical Research Council Clinical Sciences Centre, Faculty of Medicine, Imperial College London, Hammersmith Hospital)

  • Xi-Ming Sun

    (Medical Research Council Clinical Sciences Centre, Faculty of Medicine, Imperial College London, Hammersmith Hospital)

  • Anna Serafín

    (Platform of Applied Research on Laboratory Animal, Barcelona Science Park, Baldiri Reixac 4)

  • James Ware

    (Medical Research Council Clinical Sciences Centre, Faculty of Medicine, Imperial College London, Hammersmith Hospital)

  • Leonardo Bottolo

    (Medical Research Council Clinical Sciences Centre, Faculty of Medicine, Imperial College London, Hammersmith Hospital)

  • Phil Muckett

    (Medical Research Council Clinical Sciences Centre, Faculty of Medicine, Imperial College London, Hammersmith Hospital)

  • Xavier Cañas

    (Platform of Applied Research on Laboratory Animal, Barcelona Science Park, Baldiri Reixac 4)

  • Jisheng Zhang

    (Cell Signaling & Apoptosis Group, University Lleida, Biomedical Research Institute of Lleida (IRBLLEIDA), Avenida Rovira Roure 80)

  • Glenn C. Rowe

    (Cardiovascular Institute, Beth Israel Deaconess Medical Institute, CLS906, 3 Blackfan Circle)

  • Rachel Buchan

    (Medical Research Council Clinical Sciences Centre, Faculty of Medicine, Imperial College London, Hammersmith Hospital)

  • Han Lu

    (Medical Research Council Clinical Sciences Centre, Faculty of Medicine, Imperial College London, Hammersmith Hospital)

  • Adam Braithwaite

    (Medical Research Council Clinical Sciences Centre, Faculty of Medicine, Imperial College London, Hammersmith Hospital)

  • Massimiliano Mancini

    (Oncological and Anatomo-Pathological Sciences, University of Rome)

  • David Hauton

    (School of Clinical and Experimental Medicine, College of Medical and Dental Sciences, University of Birmingham, Edgbaston)

  • Ramon Martí

    (Unitat de Patologia Mitocondrial i Neuromuscular CIBERER, Institut de Recerca Hospital Universitari Vall d’Hebron, Universitat Autònoma de Barcelona)

  • Elena García-Arumí

    (Unitat de Patologia Mitocondrial i Neuromuscular CIBERER, Institut de Recerca Hospital Universitari Vall d’Hebron, Universitat Autònoma de Barcelona)

  • Norbert Hubner

    (Max-Delbrück Center for Molecular Medicine, Robert-Rössle-Strasse 10
    CC4, Campus Charité Mitte, Charité-Universitätsmedizin Berlin, Charitéplatz 1)

  • Howard Jacob

    (Medical College of Wisconsin)

  • Tadao Serikawa

    (Institute of Laboratory Animals, Graduate School of Medicine, Kyoto University, Yoshidakonoe-cho)

  • Vaclav Zidek

    (Institute of Physiology, Academy of Sciences of the Czech Republic, Vídenska 1083)

  • Frantisek Papousek

    (Institute of Physiology, Academy of Sciences of the Czech Republic, Vídenska 1083)

  • Frantisek Kolar

    (Institute of Physiology, Academy of Sciences of the Czech Republic, Vídenska 1083)

  • Maria Cardona

    (Cell Signaling & Apoptosis Group, University Lleida, Biomedical Research Institute of Lleida (IRBLLEIDA), Avenida Rovira Roure 80)

  • Marisol Ruiz-Meana

    (Grup de Patologia Cardiovascular, Institut de Recerca Hospital Universitari Vall d’Hebron, Universitat Autònoma de Barcelona, Pg. Vall d’Hebron, 119)

  • David García-Dorado

    (Grup de Patologia Cardiovascular, Institut de Recerca Hospital Universitari Vall d’Hebron, Universitat Autònoma de Barcelona, Pg. Vall d’Hebron, 119)

  • Joan X. Comella

    (Cell Signaling & Apoptosis Group at CIBERNED and Vall d’Hebron Institute of Research (VHIR), Pg. Vall d'Hebron, 119-129
    Department of Biochemistry and Molecular Biology and the Institut de Neurociencies at Universitat Autonoma de Barcelona)

  • Leanne E. Felkin

    (Heart Science Centre, National Heart and Lung Institute, Imperial College London, Harefield Hospital)

  • Paul J. R. Barton

    (Heart Science Centre, National Heart and Lung Institute, Imperial College London, Harefield Hospital
    Cardiovascular Biomedical Research Unit, Royal Brompton and Harefield NHS Trust)

  • Zoltan Arany

    (Cardiovascular Institute, Beth Israel Deaconess Medical Institute, CLS906, 3 Blackfan Circle)

  • Michal Pravenec

    (Institute of Physiology, Academy of Sciences of the Czech Republic, Vídenska 1083)

  • Enrico Petretto

    (Medical Research Council Clinical Sciences Centre, Faculty of Medicine, Imperial College London, Hammersmith Hospital
    Faculty of Medicine, Imperial College London)

  • Daniel Sanchis

    (Cell Signaling & Apoptosis Group, University Lleida, Biomedical Research Institute of Lleida (IRBLLEIDA), Avenida Rovira Roure 80)

  • Stuart A. Cook

    (Medical Research Council Clinical Sciences Centre, Faculty of Medicine, Imperial College London, Hammersmith Hospital
    Cardiovascular Biomedical Research Unit, Royal Brompton and Harefield NHS Trust)

Abstract

Endonuclease G and heart disease Elevated left ventricular mass, a highly heritable trait, is an important risk factor for heart failure and death. Stuart Cook and colleagues genetically dissect a locus in the rat associated with blood-pressure-independent cardiac hypertrophy and identify endonuclease G (ENDOG) as a key regulator of hypertrophy at this locus. They further show that the Endog gene is involved in proper mitochondrial function and is modulated by ERR-α and PGC1α, master regulators of mitochondrial and cardiac function. Loss of function of ENDOG causes impaired mitochondrial respiration and increased production of reactive oxygen species, which may contribute to the observed cardiac hypertrophy.

Suggested Citation

  • Chris McDermott-Roe & Junmei Ye & Rizwan Ahmed & Xi-Ming Sun & Anna Serafín & James Ware & Leonardo Bottolo & Phil Muckett & Xavier Cañas & Jisheng Zhang & Glenn C. Rowe & Rachel Buchan & Han Lu & Ada, 2011. "Endonuclease G is a novel determinant of cardiac hypertrophy and mitochondrial function," Nature, Nature, vol. 478(7367), pages 114-118, October.
    • Handle: RePEc:nat:nature:v:478:y:2011:i:7367:d:10.1038_nature10490
    DOI: 10.1038/nature10490
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