ArticleAmerican journal of physiology. Endocrinology and metabolism2011
Effect of postdevelopmental myostatin depletion on myofibrillar protein metabolism.
Article in American journal of physiology. Endocrinology and metabolism, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
What it found
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Who cites it
10 citing papers in PubMed, 24 citations in OpenAlex.
- Muscle-enriched microRNA-486-mediated regulation of muscular atrophy and exercise.Journal of physiology and biochemistry · 2024Review
- Muscle follistatin gene delivery increases muscle protein synthesis independent of periodical physical inactivity and fasting.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2021Article
- Androgen-mediated regulation of skeletal muscle protein balance.Molecular and cellular endocrinology · 2017Review
- Myostatin and the skeletal muscle atrophy and hypertrophy signaling pathways.Cellular and molecular life sciences : CMLS · 2014Review
- New roles for Smad signaling and phosphatidic acid in the regulation of skeletal muscle mass.F1000prime reports · 2014Review
- Myostatin inhibitors as therapies for muscle wasting associated with cancer and other disorders.Current opinion in supportive and palliative care · 2013Review
- Metabolic functions of glucocorticoid receptor in skeletal muscle.Molecular and cellular endocrinology · 2013Review
- Smad3 induces atrogin-1, inhibits mTOR and protein synthesis, and promotes muscle atrophy in vivo.Molecular endocrinology (Baltimore, Md.) · 2013Article
- Role of microRNAs in skeletal muscle hypertrophy.Frontiers in physiology · 2013Review
- Inhibition of FoxO transcriptional activity prevents muscle fiber atrophy during cachexia and induces hypertrophy.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2012Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
It is unclear whether the muscle hypertrophy induced by loss of myostatin signaling in mature muscles is maintained only by increased protein synthesis or whether reduced proteolysis contributes. To address this issue, we depleted myostatin by activating Cre recombinase for 2 wk in mature mice in which Mstn exon 3 was flanked by loxP sequences. The rate of phenylalanine tracer incorporation into myofibrillar proteins was determined 2, 5, and 24 wk after Cre activation ended. At all of these time points, myostatin-deficient mice had increased gastrocnemius and quadriceps muscle mass (≥27%) and increased myofibrillar synthesis rate per gastrocnemius muscle (≥19%) but normal myofibrillar synthesis rates per myofibrillar mass or RNA mass. Mean fractional myofibrillar degradation rates (estimated from the difference between rate of synthesis and rate of change in myofibrillar mass) and muscle concentrations of free 3-methylhistidine (from actin and myosin degradation) were unaffected by myostatin knockout. Overnight food deprivation reduced myofibrillar synthesis and ribosomal protein S6 phosphorylation and increased concentrations of 3-methylhistidine, muscle RING finger-1 mRNA, and atrogin-1 mRNA. Myostatin depletion did not affect these responses to food deprivation. These data indicate that maintenance of the muscle hypertrophy caused by loss of myostatin is mediated by increased protein synthesis per muscle fiber rather than suppression of proteolysis.
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