Abstract
Glucocorticoids inhibit protein synthesis and stimulate protein degradation in skeletal muscle and are an important factor in the development of muscle atrophy in various catabolic conditions. Glucocorticoid-stimulated muscle protein breakdown is primarily caused by ubiquitin-proteasome-dependent proteolysis although calcium-dependent protein degradation may also be involved. In certain catabolic conditions, including sepsis, an interaction between glucocorticoids and proinflammatory cytokines is important for the stimulation of muscle protein breakdown.
Publication types
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Research Support, Non-U.S. Gov't
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Research Support, U.S. Gov't, P.H.S.
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Review
MeSH terms
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Aging / metabolism
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Animals
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Cushing Syndrome / genetics
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Cysteine Endopeptidases / metabolism
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Cytokines / metabolism
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Gene Expression
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Glucocorticoids / pharmacology*
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Glutamate-Ammonia Ligase / metabolism
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Humans
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Multienzyme Complexes / metabolism
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Muscles / drug effects*
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Muscles / metabolism*
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Muscles / physiopathology
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Proteasome Endopeptidase Complex
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Ubiquitins / metabolism
Substances
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Cytokines
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Glucocorticoids
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Multienzyme Complexes
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Ubiquitins
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Cysteine Endopeptidases
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Proteasome Endopeptidase Complex
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Glutamate-Ammonia Ligase