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Saleem A.,Muscle Health Research Center | Carter H.N.,Muscle Health Research Center | Iqbal S.,Muscle Health Research Center | Hood D.A.,Muscle Health Research Center | Hood D.A.,York University
Exercise and Sport Sciences Reviews

The tumor suppressor protein p53 is recognized to contribute significantly to the regulation of mitochondrial content. Mice without p53 have reduced endurance capacity and muscle performance. However, the function of p53 in muscle remains to be fully established. Understanding how p53 coordinates mitochondrial homeostasis will facilitate a better comprehension of how exercise could constitute as a therapy for cancer treatment. © 2011 by the American College of Sports Medicine. Source

Huang J.H.,York University | Huang J.H.,Muscle Health Research Center | Joseph A.-M.,Muscle Health Research Center | Joseph A.-M.,York University | And 6 more authors.
Journals of Gerontology - Series A Biological Sciences and Medical Sciences

Deregulation of muscle mitochondrial biogenesis may explain the altered mitochondrial properties associated with aging. Maintenance of the mitochondrial network requires the continuous incorporation of nascent proteins into their subcompartments via the protein import pathway. We examined whether this pathway was impaired in muscle of aged animals, focusing on the subsarcolemmal and intermyofibrillar mitochondrial populations. Our results indicate that the import of proteins into the mitochondrial matrix was unaltered with age. Interestingly, import assays supplemented with the cytosolic fraction illustrated an attenuation of protein import, and this effect was similar between age groups. We observed a 2.5-fold increase in protein degradation in the presence of the cytosolic fraction obtained from aged animals. Thus, the reduction of mitochondrial content and/or function observed with aging may not rely on altered activity of the import pathway but rather on the availability of preproteins that are susceptible to elevated rates of degradation by cytosolic factors. Source

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