Myokine mediated muscle-kidney crosstalk suppresses metabolic reprogramming and fibrosis in damaged kidneys
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...
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| Published in | Nature communications Vol. 8; no. 1; pp. 1493 - 15 |
|---|---|
| Main Authors | , , , , , , , , , , , |
| Format | Journal Article |
| Language | English |
| Published |
London
Nature Publishing Group UK
14.11.2017
Nature Publishing Group Nature Portfolio |
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| 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.
Progressive tubule cell damage results in defects in mitochondrial metabolism and exercise seems to be beneficial during chronic kidney disease. Here Peng et al. show that irisin, an exercise-induced myokine, improves kidney energy metabolism by inhibiting TGF-β type 1 receptors and ameliorates fibrosis. |
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| AbstractList | 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.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. 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. Progressive tubule cell damage results in defects in mitochondrial metabolism and exercise seems to be beneficial during chronic kidney disease. Here Peng et al. show that irisin, an exercise-induced myokine, improves kidney energy metabolism by inhibiting TGF-β type 1 receptors and ameliorates fibrosis. 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. Progressive tubule cell damage results in defects in mitochondrial metabolism and exercise seems to be beneficial during chronic kidney disease. Here Peng et al. show that irisin, an exercise-induced myokine, improves kidney energy metabolism by inhibiting TGF-β type 1 receptors and ameliorates fibrosis. |
| ArticleNumber | 1493 |
| Author | Wang, Qianqian Wang, Yanlin Feng, Xin-hua Graham, Brett H. Mitch, William E. Qin, Jun Li, Feng Shetty, Vivekananda Jung, Sungyun Hu, Zhaoyong Lou, Tanqi Peng, Hui |
| Author_xml | – sequence: 1 givenname: Hui surname: Peng fullname: Peng, Hui organization: Nephrology Division, the Third Affiliated Hospital of Sun Yat-sen University, Nephrology Division, Department of Medicine, Baylor College of Medicine – sequence: 2 givenname: Qianqian surname: Wang fullname: Wang, Qianqian organization: Nephrology Division, the Third Affiliated Hospital of Sun Yat-sen University, Nephrology Division, Department of Medicine, Baylor College of Medicine – sequence: 3 givenname: Tanqi surname: Lou fullname: Lou, Tanqi organization: Nephrology Division, the Third Affiliated Hospital of Sun Yat-sen University – sequence: 4 givenname: Jun surname: Qin fullname: Qin, Jun organization: Department of Biochemistry and Molecular Biology, Baylor College of Medicine – sequence: 5 givenname: Sungyun surname: Jung fullname: Jung, Sungyun organization: Department of Biochemistry and Molecular Biology, Baylor College of Medicine – sequence: 6 givenname: Vivekananda surname: Shetty fullname: Shetty, Vivekananda organization: The Metabolomics and Proteomics Core, Baylor College of Medicine – sequence: 7 givenname: Feng surname: Li fullname: Li, Feng organization: The Metabolomics and Proteomics Core, Baylor College of Medicine – sequence: 8 givenname: Yanlin surname: Wang fullname: Wang, Yanlin organization: Nephrology Division, Department of Medicine, Baylor College of Medicine – sequence: 9 givenname: Xin-hua surname: Feng fullname: Feng, Xin-hua organization: Department of Surgery, Baylor College of Medicine – sequence: 10 givenname: William E. surname: Mitch fullname: Mitch, William E. organization: Nephrology Division, Department of Medicine, Baylor College of Medicine – sequence: 11 givenname: Brett H. orcidid: 0000-0001-8451-8154 surname: Graham fullname: Graham, Brett H. organization: Department of Molecular and Human Genetics, Baylor College of Medicine – sequence: 12 givenname: Zhaoyong surname: Hu fullname: Hu, Zhaoyong email: zhaoyonh@bcm.edu organization: Nephrology Division, Department of Medicine, Baylor College of Medicine |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/29138395$$D View this record in MEDLINE/PubMed |
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| Snippet | Kidney injury initiates metabolic reprogramming in tubule cells that contributes to the development of chronic kidney disease (CKD). Exercise has been... Progressive tubule cell damage results in defects in mitochondrial metabolism and exercise seems to be beneficial during chronic kidney disease. Here Peng et... |
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| SubjectTerms | 692/4022/1585/3182 692/699/1585/104 Crosstalk Damage prevention Energy metabolism Fibrosis Humanities and Social Sciences Injury analysis Injury prevention Kidney diseases Kidney transplantation Kidneys Metabolism Metabolomics Mice multidisciplinary Oxygen consumption Rodents Science Science (multidisciplinary) |
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| Title | Myokine mediated muscle-kidney crosstalk suppresses metabolic reprogramming and fibrosis in damaged kidneys |
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