| First Author | Pérez-Schindler J | Year | 2013 |
| Journal | Proc Natl Acad Sci U S A | Volume | 110 |
| Issue | 50 | Pages | 20314-9 |
| PubMed ID | 24277823 | Mgi Jnum | J:205184 |
| Mgi Id | MGI:5544347 | Doi | 10.1073/pnas.1312039110 |
| Citation | Perez-Schindler J, et al. (2013) The transcriptional coactivator PGC-1alpha is dispensable for chronic overload-induced skeletal muscle hypertrophy and metabolic remodeling. Proc Natl Acad Sci U S A 110(50):20314-9 |
| abstractText | Skeletal muscle mass loss and dysfunction have been linked to many diseases. Conversely, resistance exercise, mainly by activating mammalian target of rapamycin complex 1 (mTORC1), promotes skeletal muscle hypertrophy and exerts several therapeutic effects. Moreover, mTORC1, along with peroxisome proliferator-activated receptor gamma coactivator 1alpha (PGC-1alpha), regulates skeletal muscle metabolism. However, it is unclear whether PGC-1alpha is required for skeletal muscle adaptations after overload. Here we show that although chronic overload of skeletal muscle via synergist ablation (SA) strongly induces hypertrophy and a switch toward a slow-contractile phenotype, these effects were independent of PGC-1alpha. In fact, SA down-regulated PGC-1alpha expression and led to a repression of energy metabolism. Interestingly, however, PGC-1alpha deletion preserved peak force after SA. Taken together, our data suggest that PGC-1alpha is not involved in skeletal muscle remodeling induced by SA. |
