Skip to main content

Research Repository

Advanced Search

All Outputs (44)

Altered Primary and Secondary Myogenesis in the Myostatin-Null Mouse (2010)
Journal Article
Matsakas, A., Otto, A., Elashry, M. I., Brown, S. C., & Patel, K. (2010). Altered Primary and Secondary Myogenesis in the Myostatin-Null Mouse. Rejuvenation Research, 13(6), 717-727. https://doi.org/10.1089/rej.2010.1065

Skeletal muscle fiber generation occurs principally in two myogenic phases: (1) Primary (embryonic) myogenesis when myoblasts proliferate and fuse to form primary myotubes and (2) secondary (fetal) myogenesis when successive waves of myoblasts fuse a... Read More about Altered Primary and Secondary Myogenesis in the Myostatin-Null Mouse.

Myostatin knockout mice increase oxidative muscle phenotype as an adaptive response to exercise (2010)
Journal Article
Matsakas, A., Mouisel, E., Amthor, H., & Patel, K. (2010). Myostatin knockout mice increase oxidative muscle phenotype as an adaptive response to exercise. Journal of Muscle Research and Cell Motility, 31(2), 111-125. https://doi.org/10.1007/s10974-010-9214-9

Myostatin-deficient mice (MSTN (-/-)) display excessive muscle mass and this is associated with a profound loss of oxidative metabolic properties. In this study we analysed the effect of two endurance-based exercise regimes, either a forced high-impa... Read More about Myostatin knockout mice increase oxidative muscle phenotype as an adaptive response to exercise.

A hypoplastic model of skeletal muscle development displaying reduced foetal myoblast cell numbers, increased oxidative myofibres and improved specific tension capacity (2010)
Journal Article
Otto, A., Macharia, R., Matsakas, A., Valasek, P., Mankoo, B. S., & Patel, K. (2010). A hypoplastic model of skeletal muscle development displaying reduced foetal myoblast cell numbers, increased oxidative myofibres and improved specific tension capacity. Developmental Biology, 343(1-2), 51-62. https://doi.org/10.1016/j.ydbio.2010.04.014

The major component of skeletal muscle is the myofibre. Genetic intervention inducing over-enlargement of myofibres beyond a certain threshold through acellular growth causes a reduction in the specific tension generating capacity of the muscle. Howe... Read More about A hypoplastic model of skeletal muscle development displaying reduced foetal myoblast cell numbers, increased oxidative myofibres and improved specific tension capacity.

Muscle hypertrophy driven by myostatin blockade does not require stem/precursor-cell activity (2009)
Journal Article
Amthor, H., Otto, A., Vulin, A., Rochat, A., Dumonceaux, J., Garcia, L., Mouisel, E., Hourdé, C., Macharia, R., Friedrichs, M., Relaix, F., Zammit, P. S., Matsakas, A., Patel, K., & Partridge, T. (2009). Muscle hypertrophy driven by myostatin blockade does not require stem/precursor-cell activity. Proceedings of the National Academy of Sciences of the United States of America, 106(18), 7479-7484. https://doi.org/10.1073/pnas.0811129106

Myostatin, a member of the TGF-β family, has been identified as a powerful inhibitor of muscle growth. Absence or blockade of myostatin induces massive skeletal muscle hypertrophy that is widely attributed to proliferation of the population of muscle... Read More about Muscle hypertrophy driven by myostatin blockade does not require stem/precursor-cell activity.