| First Author | Gali Ramamoorthy T | Year | 2015 |
| Journal | Nat Commun | Volume | 6 |
| Pages | 10210 | PubMed ID | 26674215 |
| Mgi Jnum | J:228281 | Mgi Id | MGI:5706649 |
| Doi | 10.1038/ncomms10210 | Citation | Gali Ramamoorthy T, et al. (2015) The transcriptional coregulator PGC-1beta controls mitochondrial function and anti-oxidant defence in skeletal muscles. Nat Commun 6:10210 |
| abstractText | The transcriptional coregulators PGC-1alpha and PGC-1beta modulate the expression of numerous partially overlapping genes involved in mitochondrial biogenesis and energetic metabolism. The physiological role of PGC-1beta is poorly understood in skeletal muscle, a tissue of high mitochondrial content to produce ATP levels required for sustained contractions. Here we determine the physiological role of PGC-1beta in skeletal muscle using mice, in which PGC-1beta is selectively ablated in skeletal myofibres at adulthood (PGC-1beta((i)skm-/-) mice). We show that myofibre myosin heavy chain composition and mitochondrial number, muscle strength and glucose homeostasis are unaffected in PGC-1beta((i)skm-/-) mice. However, decreased expression of genes controlling mitochondrial protein import, translational machinery and energy metabolism in PGC-1beta((i)skm-/-) muscles leads to mitochondrial structural and functional abnormalities, impaired muscle oxidative capacity and reduced exercise performance. Moreover, enhanced free-radical leak and reduced expression of the mitochondrial anti-oxidant enzyme Sod2 increase muscle oxidative stress. PGC-1beta is therefore instrumental for skeletal muscles to cope with high energetic demands. |
