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Ageing and disuse represent two of the most prevalent and costly atrophic conditions, with resistance exercise training (RET) being the most effective lifestyle countermeasure. We employed gene\u2010level and network\u2010level meta\u2010analyses to contrast transcriptomic signatures of disuse and RET, plus young and older RET to establish a consensus on the molecular features of, and therapeutic targets against, muscle atrophy in conditions of high socio\u2010economic relevance.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>\n                      Integrated gene\u2010level and network\u2010level meta\u2010analysis was performed on publicly available microarray data sets generated from young (18\u201335\u00a0years)\n                      <jats:italic>m. vastus lateralis<\/jats:italic>\n                      muscle subjected to disuse (unilateral limb immobilization or bed rest) lasting \u22657\u00a0days or RET lasting \u22653\u00a0weeks, and resistance\u2010trained older (\u226560\u00a0years) muscle.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>\n                      Disuse and RET displayed predominantly separate transcriptional responses, and transcripts altered across conditions were mostly unidirectional. However, disuse and RET induced directly inverted expression profiles for mitochondrial function and translation regulation genes, with\n                      <jats:italic>COX4I1<\/jats:italic>\n                      ,\n                      <jats:italic>ENDOG<\/jats:italic>\n                      ,\n                      <jats:italic>GOT2<\/jats:italic>\n                      ,\n                      <jats:italic>MRPL12<\/jats:italic>\n                      , and\n                      <jats:italic>NDUFV2<\/jats:italic>\n                      , the central hub components of altered mitochondrial networks, and\n                      <jats:italic>ZMYND11<\/jats:italic>\n                      , a hub gene of altered translation regulation. A substantial number of genes (\n                      <jats:italic>n<\/jats:italic>\n                      \u00a0=\u00a0140) up\u2010regulated post\u2010RET in younger muscle were not similarly up\u2010regulated in older muscle, with young muscle displaying a more pronounced extracellular matrix (ECM) and immune\/inflammatory gene expression response. Both young and older muscle exhibited similar RET\u2010induced ubiquitination\/RNA processing gene signatures with associated\n                      <jats:italic>PWP1<\/jats:italic>\n                      ,\n                      <jats:italic>PSMB1<\/jats:italic>\n                      , and\n                      <jats:italic>RAF1<\/jats:italic>\n                      hub genes.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusions<\/jats:title>\n                    <jats:p>Despite limited opposing gene profiles, transcriptional signatures of disuse are not simply the converse of RET. Thus, the mechanisms of unloading cannot be derived from studying muscle loading alone and provides a molecular basis for understanding why RET fails to target all transcriptional features of disuse. Loss of RET\u2010induced ECM mechanotransduction and inflammatory profiles might also contribute to suboptimal ageing muscle adaptations to RET. Disuse and age\u2010dependent molecular candidates further establish a framework for understanding and treating disuse\/ageing atrophy.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1002\/jcsm.12706","type":"journal-article","created":{"date-parts":[[2021,5,6]],"date-time":"2021-05-06T02:47:48Z","timestamp":1620269268000},"page":"629-645","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":44,"title":["Transcriptomic meta\u2010analysis of disuse muscle atrophy vs. resistance exercise\u2010induced hypertrophy in young and older humans"],"prefix":"10.1002","volume":"12","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-2281-6479","authenticated-orcid":false,"given":"Colleen S.","family":"Deane","sequence":"first","affiliation":[{"name":"Department of Sport and Health Sciences, College of Life and Environmental Sciences University of Exeter, St. Luke's Campus  Exeter UK"},{"name":"Living Systems Institute University of Exeter 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