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| Content Provider | World Health Organization (WHO)-Global Index Medicus |
|---|---|
| Author | Li, Hong Mittal, Ashwani Bhatnagar, Shephali Lach-trifilieff, Estelle Wauters, Sandrine Glass, David J. Makonchuk, Denys Y. Kumar, Ashok Kumar, Akhilesh |
| Description | Author Affiliation: Mittal A ( Department of Anatomical Sciences and Neurobiology, University of Louisville School of Medicine, Louisville, KY 40202, USA.) |
| Abstract | Skeletal muscle atrophy occurs in a variety of clinical settings, including cachexia, disuse, and denervation. Inflammatory cytokines have been shown to be mediators of cancer cachexia; however, the role of cytokines in denervation- and immobilization-induced skeletal muscle loss remains unknown. In this study, we demonstrate that a single cytokine, TNF-like weak inducer of apoptosis (TWEAK), mediates skeletal muscle atrophy that occurs under denervation conditions. Transgenic expression of TWEAK induces atrophy, fibrosis, fiber-type switching, and the degradation of muscle proteins. Importantly, genetic ablation of TWEAK decreases the loss of muscle proteins and spared fiber cross-sectional area, muscle mass, and strength after denervation. Expression of the TWEAK receptor Fn14 (fibroblast growth factor–inducible receptor 14) and not the cytokine is significantly increased in muscle upon denervation, demonstrating an unexpected inside-out signaling pathway; the receptor up-regulation allows for TWEAK activation of nuclear factor κB, causing an increase in the expression of the E3 ubiquitin ligase MuRF1. This study reveals a novel mediator of skeletal muscle atrophy and indicates that the TWEAK–Fn14 system is an important target for preventing skeletal muscle wasting. |
| ISSN | 00219525 |
| e-ISSN | 15408140 |
| Journal | The Journal of Cell Biology |
| Issue Number | 6 |
| Volume Number | 188 |
| Language | English |
| Publisher | Rockefeller University Press (United States) |
| Publisher Date | 2010-03-22 |
| Publisher Place | United States |
| Access Restriction | Open |
| Subject Keyword | Muscle, Skeletal Metabolism Pathology Muscular Atrophy Receptors, Tumor Necrosis Factor Tumor Necrosis Factors Animals Disease Models, Animal Mice Mice, Inbred C57BL Mice, Knockout Mice, Transgenic Muscle Denervation Reverse Transcriptase Polymerase Chain Reaction Deficiency Genetics Research Support, N.I.H., Extramural Cell Biology |
| Content Type | Text |
| Resource Type | Article |
| Subject | Cell Biology Medicine |
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