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

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 and Zhaoyong Hu ()
Additional contact information
Hui Peng: the Third Affiliated Hospital of Sun Yat-sen University
Qianqian Wang: the Third Affiliated Hospital of Sun Yat-sen University
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

Nature Communications, 2017, vol. 8, issue 1, 1-15

Abstract: 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.

Date: 2017
References: Add references at CitEc
Citations: View citations in EconPapers (1)

Downloads: (external link)
https://www.nature.com/articles/s41467-017-01646-6 Abstract (text/html)

Related works:
This item may be available elsewhere in EconPapers: Search for items with the same title.

Export reference: BibTeX RIS (EndNote, ProCite, RefMan) HTML/Text

Persistent link: https://EconPapers.repec.org/RePEc:nat:natcom:v:8:y:2017:i:1:d:10.1038_s41467-017-01646-6

Ordering information: This journal article can be ordered from
https://www.nature.com/ncomms/

DOI: 10.1038/s41467-017-01646-6

Access Statistics for this article

Nature Communications is currently edited by Nathalie Le Bot, Enda Bergin and Fiona Gillespie

More articles in Nature Communications from Nature
Bibliographic data for series maintained by Sonal Shukla () and Springer Nature Abstracting and Indexing ().