PGC-1α overexpression partially rescues impaired oxidative and contractile pathophysiology following volumetric muscle loss injury
Author:
Funder
U.S. Department of Health & Human Services | National Institutes of Health
U.S. Department of Defense
Publisher
Springer Science and Business Media LLC
Subject
Multidisciplinary
Link
http://www.nature.com/articles/s41598-019-40606-6.pdf
Reference71 articles.
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2. Ingjer, F. Effects of endurance training on muscle fibre ATP-ase activity, capillary supply and mitochondrial content in man. J. Physiol. 294, 419–432 (1979).
3. Hood, D. A., Tryon, L. D., Carter, H. N., Kim, Y. & Chen, C. C. Unravelling the mechanisms regulating muscle mitochondrial biogenesis. Biochem. J. 473, 2295–2314, https://doi.org/10.1042/BCJ20160009 (2016).
4. Arnold, A. S. et al. Morphological and functional remodelling of the neuromuscular junction by skeletal muscle PGC-1alpha. Nat. Commun. 5, 3569, https://doi.org/10.1038/ncomms4569 (2014).
5. Fernandez-Marcos, P. J. & Auwerx, J. Regulation of PGC-1alpha, a nodal regulator of mitochondrial biogenesis. Am. J. Clin. Nutr. 93, 884S–890, https://doi.org/10.3945/ajcn.110.001917 (2011).
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