IDEAS home Printed from https://ideas.repec.org/a/nat/natcom/v8y2017i1d10.1038_s41467-017-01646-6.html
   My bibliography  Save this article

Myokine mediated muscle-kidney crosstalk suppresses metabolic reprogramming and fibrosis in damaged kidneys

Author

Listed:
  • Hui Peng

    (the Third Affiliated Hospital of Sun Yat-sen University
    Department of Medicine, Baylor College of Medicine)

  • Qianqian Wang

    (the Third Affiliated Hospital of Sun Yat-sen University
    Department of Medicine, Baylor College of Medicine)

  • Tanqi Lou

    (the Third Affiliated Hospital of Sun Yat-sen University)

  • Jun Qin

    (Baylor College of Medicine)

  • Sungyun Jung

    (Baylor College of Medicine)

  • Vivekananda Shetty

    (Baylor College of Medicine)

  • Feng Li

    (Baylor College of Medicine)

  • Yanlin Wang

    (Department of Medicine, Baylor College of Medicine)

  • Xin-hua Feng

    (Baylor College of Medicine)

  • William E. Mitch

    (Department of Medicine, Baylor College of Medicine)

  • Brett H. Graham

    (Baylor College of Medicine)

  • Zhaoyong Hu

    (Department of Medicine, Baylor College of Medicine)

Abstract

Kidney injury initiates metabolic reprogramming in tubule cells that contributes to the development of chronic kidney disease (CKD). Exercise has been associated with beneficial effects in patients with CKD. Here we show that the induction of a myokine, irisin, improves kidney energy metabolism and prevents kidney damage. In response to kidney injury, mice with muscle-specific PGC-1α overexpression (mPGC-1α) exhibit reduced kidney damage and fibrosis. Metabolomics analysis reveals increased ATP production and improved energy metabolism in injured kidneys from mPGC-1α mice. We identify irisin as a serum factor that mediates these metabolic effects during progressive kidney injury by inhibiting TGF-β type 1 receptor. Irisin depletion from serum blunts the induction of oxygen consumption rate observed in tubule cells treated with mPGC-1α serum. In mice, recombinant irisin administration attenuates kidney damage and fibrosis and improves kidney functions. We suggest that myokine-mediated muscle-kidney crosstalk can suppress metabolic reprograming and fibrogenesis during kidney disease.

Suggested Citation

  • Hui Peng & Qianqian Wang & Tanqi Lou & Jun Qin & Sungyun Jung & Vivekananda Shetty & Feng Li & Yanlin Wang & Xin-hua Feng & William E. Mitch & Brett H. Graham & Zhaoyong Hu, 2017. "Myokine mediated muscle-kidney crosstalk suppresses metabolic reprogramming and fibrosis in damaged kidneys," Nature Communications, Nature, vol. 8(1), pages 1-15, December.
    • Handle: RePEc:nat:natcom:v:8:y:2017:i:1:d:10.1038_s41467-017-01646-6
    DOI: 10.1038/s41467-017-01646-6
    as

    Download full text from publisher

    File URL: https://www.nature.com/articles/s41467-017-01646-6
    File Function: Abstract
    Download Restriction: no
    File URL: https://libkey.io/10.1038/s41467-017-01646-6?utm_source=ideas
    LibKey link: if access is restricted and if your library uses this service, LibKey will redirect you to where you can use your library subscription to access this item
    ---><---

    Citations

    Citations are extracted by the CitEc Project, subscribe to its RSS feed for this item.
    as


    Cited by:

    1. Yunwen Yang & Suwen Liu & Peipei Wang & Jing Ouyang & Ning Zhou & Yue Zhang & Songming Huang & Zhanjun Jia & Aihua Zhang, 2023. "DNA-dependent protein kinase catalytic subunit (DNA-PKcs) drives chronic kidney disease progression in male mice," Nature Communications, Nature, vol. 14(1), pages 1-17, December.

    More about this item

    Statistics

    Access and download statistics

    Corrections

    All material on this site has been provided by the respective publishers and authors. You can help correct errors and omissions. When requesting a correction, please mention this item's handle: RePEc:nat:natcom:v:8:y:2017:i:1:d:10.1038_s41467-017-01646-6. See general information about how to correct material in RePEc.

    If you have authored this item and are not yet registered with RePEc, we encourage you to do it here. This allows to link your profile to this item. It also allows you to accept potential citations to this item that we are uncertain about.

    We have no bibliographic references for this item. You can help adding them by using this form .

    If you know of missing items citing this one, you can help us creating those links by adding the relevant references in the same way as above, for each refering item. If you are a registered author of this item, you may also want to check the "citations" tab in your RePEc Author Service profile, as there may be some citations waiting for confirmation.

    For technical questions regarding this item, or to correct its authors, title, abstract, bibliographic or download information, contact: Sonal Shukla or Springer Nature Abstracting and Indexing (email available below). General contact details of provider: http://www.nature.com .

    Please note that corrections may take a couple of weeks to filter through the various RePEc services.

    IDEAS is a RePEc service. RePEc uses bibliographic data supplied by the respective publishers.