{"doi":"10.1002/mus.20888","title":"Effects of nandrolone on denervation atrophy depend upon time after nerve transection","abstract":"<jats:title>Abstract</jats:title><jats:p>Anabolic steroids prevent disuse atrophy and reverse atrophy caused by glucocorticoids. To determine whether these beneficial effects extend to denervation atrophy, we tested whether nandrolone blocked denervation atrophy acutely or reversed subacute denervation atrophy. We also tested the association of such anabolic effects with expression of MAFbx, MuRF1 (both of which accelerate denervation atrophy), and IGF‐1 (which prevents such atrophy). When begun at the time of denervation, nandrolone did not alter atrophy or expression of MAFbx, MuRF1, or IGF‐1 measured 3, 7, or 14 days thereafter. When nandrolone administration was begun 28 days after denervation, atrophy was significantly reduced 7 and 28 days later (16% and 30%, respectively), and this was associated with significant reductions in expression of MAFbx and MuRF1, without alterations in the expression of IGF‐1. The findings indicate that the actions of nandrolone depend on time after nerve transection and that the timing of anabolic steroid administration is an important determinant of responses of atrophying muscle to these agents. Muscle Nerve, 2007</jats:p>","journal":"Muscle &amp; Nerve","year":2008,"id":683969,"datarank":0.5495342469194471,"base_score":3.6635616461296463,"endowment":3.6635616461296463,"self_citation_contribution":0.5495342469194471,"citation_network_contribution":0.0,"self_endowment_contribution":0.5495342469194471,"citer_contribution":0.0,"corpus_percentile":null,"corpus_rank":null,"citation_count":38,"citer_count":0,"citers_with_citation_signal":0,"citers_with_endowment":0,"datacite_reuse_total":0,"is_dataset":false,"is_dataset_confidence":null,"is_data_producer":false,"deposit_databanks":null,"is_oa":false,"file_count":0,"downloads":0,"has_version_chain":false,"published_date":null,"fair_score":null,"fair_percentile":null,"algorithm_id":"datarank_citation_only_1hop_v6","ranking_scope":"data_only","authors":[{"id":1786827,"name":"Yuangfei Zhang","orcid":null,"position":1,"is_corresponding":false},{"id":1540947,"name":"Weidong Zhao","orcid":null,"position":2,"is_corresponding":false},{"id":1241748,"name":"Yong Wu","orcid":"0000-0001-6770-1328","position":3,"is_corresponding":false},{"id":372853,"name":"Jiangping Pan","orcid":null,"position":4,"is_corresponding":false},{"id":371582,"name":"William A. Bauman","orcid":"0000-0002-6724-7150","position":5,"is_corresponding":false},{"id":371580,"name":"Christopher Cardozo","orcid":"0000-0003-4013-2537","position":6,"is_corresponding":false},{"id":1667021,"name":"Jingbo Zhao","orcid":null,"position":0,"is_corresponding":false}],"reference_count":0,"raw_metadata":{"has_enrichment":true,"resolved":true,"title":"Effects of nandrolone on denervation atrophy depend upon time after nerve transection","abstract":"<jats:title>Abstract</jats:title><jats:p>Anabolic steroids prevent disuse atrophy and reverse atrophy caused by glucocorticoids. To determine whether these beneficial effects extend to denervation atrophy, we tested whether nandrolone blocked denervation atrophy acutely or reversed subacute denervation atrophy. We also tested the association of such anabolic effects with expression of MAFbx, MuRF1 (both of which accelerate denervation atrophy), and IGF‐1 (which prevents such atrophy). When begun at the time of denervation, nandrolone did not alter atrophy or expression of MAFbx, MuRF1, or IGF‐1 measured 3, 7, or 14 days thereafter. When nandrolone administration was begun 28 days after denervation, atrophy was significantly reduced 7 and 28 days later (16% and 30%, respectively), and this was associated with significant reductions in expression of MAFbx and MuRF1, without alterations in the expression of IGF‐1. The findings indicate that the actions of nandrolone depend on time after nerve transection and that the timing of anabolic steroid administration is an important determinant of responses of atrophying muscle to these agents. 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