IDEAS home Printed from https://ideas.repec.org/a/nat/natcom/v16y2025i1d10.1038_s41467-025-59959-w.html
   My bibliography  Save this article

Exercise-induced CLCF1 attenuates age-related muscle and bone decline in mice

Author

Listed:
  • Jae Sook Kang

    (Korea Research Institute of Bioscience and Biotechnology (KRIBB)
    Korea University of Science and Technology (UST))

  • Jung Ha Kim

    (Chonnam National University Medical School)

  • Min Ju Kim

    (Korea Research Institute of Bioscience and Biotechnology (KRIBB)
    Korea University of Science and Technology (UST))

  • Byungkuk Min

    (Korea Research Institute of Bioscience and Biotechnology (KRIBB))

  • Seung-Min Lee

    (Korea Research Institute of Bioscience and Biotechnology (KRIBB))

  • Ga-Yeon Go

    (Korea Research Institute of Bioscience and Biotechnology (KRIBB))

  • Ji-Won Kim

    (Korea Research Institute of Bioscience and Biotechnology (KRIBB))

  • Seongwan Kim

    (Korea Research Institute of Bioscience and Biotechnology (KRIBB)
    Korea University of Science and Technology (UST))

  • Ju Yeon Kwak

    (Korea Research Institute of Bioscience and Biotechnology (KRIBB))

  • Sung-Wook Chun

    (Pusan National University)

  • Wook Song

    (Seoul National University
    Seoul National University)

  • Hyo Youl Moon

    (Seoul National University
    Seoul National University)

  • Sun Gun Chung

    (Seoul National University
    Seoul National University College of Medicine)

  • Dong-Ho Park

    (Inha University
    Inha University)

  • Ji Hoon Park

    (Osong Medical Innovation Foundation (KBioHealth))

  • Chuna Kim

    (Korea Research Institute of Bioscience and Biotechnology (KRIBB)
    Korea University of Science and Technology (UST))

  • Kwang-Pyo Lee

    (Korea Research Institute of Bioscience and Biotechnology (KRIBB)
    Korea University of Science and Technology (UST))

  • Eun-Soo Kwon

    (Korea Research Institute of Bioscience and Biotechnology (KRIBB)
    Korea University of Science and Technology (UST))

  • Nacksung Kim

    (Chonnam National University Medical School)

  • Ki-Sun Kwon

    (Korea Research Institute of Bioscience and Biotechnology (KRIBB)
    Aventi Inc.)

  • Yong Ryoul Yang

    (Korea Research Institute of Bioscience and Biotechnology (KRIBB)
    Korea University of Science and Technology (UST))

Abstract

Skeletal muscle undergoes many alterations with aging. However, the impact of aging on muscle’s ability to secrete myokines and its subsequent effects on the body remain largely unexplored. Here, we identify myokines that have the potential to ameliorate age-related muscle and bone decline. Notably, circulating levels of cardiotrophin-like cytokine factor 1 (CLCF1) decrease with age, while exercise significantly upregulates CLCF1 levels in both humans and rodents. Restoring CLCF1 levels in aged male mice improves their physical performance, glucose tolerance, and mitochondrial activity. Furthermore, CLCF1 protects against age-induced bone loss by inhibiting osteoclastogenesis and promoting osteoblast differentiation in aged male mice. These improvements mirror some of the effects of exercise training. Conversely, blocking CLCF1 activity significantly abolishes these beneficial effects, confirming the crucial role of CLCF1 in mediating the positive effects of exercise on muscle and bone health in male mice. These findings collectively suggest that CLCF1 may contribute to the regulation of age-associated musculoskeletal deterioration, and warrant further investigation into its potential role as a modulator of musculoskeletal health during aging.

Suggested Citation

  • Jae Sook Kang & Jung Ha Kim & Min Ju Kim & Byungkuk Min & Seung-Min Lee & Ga-Yeon Go & Ji-Won Kim & Seongwan Kim & Ju Yeon Kwak & Sung-Wook Chun & Wook Song & Hyo Youl Moon & Sun Gun Chung & Dong-Ho P, 2025. "Exercise-induced CLCF1 attenuates age-related muscle and bone decline in mice," Nature Communications, Nature, vol. 16(1), pages 1-20, December.
  • Handle: RePEc:nat:natcom:v:16:y:2025:i:1:d:10.1038_s41467-025-59959-w
    DOI: 10.1038/s41467-025-59959-w
    as

    Download full text from publisher

    File URL: https://www.nature.com/articles/s41467-025-59959-w
    File Function: Abstract
    Download Restriction: no

    File URL: https://libkey.io/10.1038/s41467-025-59959-w?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
    ---><---

    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:16:y:2025:i:1:d:10.1038_s41467-025-59959-w. 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.