{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,27]],"date-time":"2026-10-27T20:24:56Z","timestamp":1793132696907,"version":"4.5.0"},"reference-count":43,"publisher":"Wiley","issue":"4","license":[{"start":{"date-parts":[[2025,7,10]],"date-time":"2025-07-10T00:00:00Z","timestamp":1752105600000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"funder":[{"DOI":"10.13039\/501100001809","name":"National Natural Science Foundation of China","doi-asserted-by":"publisher","id":[{"id":"10.13039\/501100001809","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100013105","name":"Shanghai Rising-Star Program","doi-asserted-by":"publisher","id":[{"id":"10.13039\/501100013105","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100003399","name":"Science and Technology Commission of Shanghai Municipality","doi-asserted-by":"publisher","id":[{"id":"10.13039\/501100003399","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100007219","name":"Natural Science Foundation of Shanghai Municipality","doi-asserted-by":"publisher","id":[{"id":"10.13039\/100007219","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100002858","name":"China Postdoctoral Science Foundation","doi-asserted-by":"publisher","id":[{"id":"10.13039\/501100002858","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["J cachexia sarcopenia muscle"],"published-print":{"date-parts":[[2025,8]]},"abstract":"<jats:title>ABSTRACT<\/jats:title><jats:sec><jats:title>Background<\/jats:title><jats:p>Muscle atrophy has a poor prognosis, caused by various factors. Identifying a shared treatment target could address an unmet clinical need. The exon junction complex (EJC), a protein complex assembly that binds to RNA, facilitates post\u2010transcriptional regulation by participating in mRNA splicing, mRNA export, translation and nonsense\u2010mediated mRNA decay. This study aims to investigate the role of the EJC in muscle atrophy.<\/jats:p><\/jats:sec><jats:sec><jats:title>Methods<\/jats:title><jats:p>Single\u2010cell transcriptome analysis and western blot were employed to analyse EJC expression in muscle atrophy. Overexpression of EJC helicase EIF4A3, as well as counteracting endogenous EIF4A3, was manipulated using lentiviral and adeno\u2010associated virus 8 (AAV8) at both in\u00a0vitro and in\u00a0vivo levels. Imaging, RT\u2010qPCR and immunoblot were utilized to identify phenotypes associated with muscle atrophy and aging. RNA\u2010seq, RIP\u2010seq, RT\u2010qPCR and RIP\u2010PCR were conducted to determine the targets of EIF4A3. A pharmacological approach that activates the downstream pathways in EIF4A3 knockdown muscle was employed to elucidate the molecular mechanisms of EIF4A3 in muscle atrophy.<\/jats:p><\/jats:sec><jats:sec><jats:title>Results<\/jats:title><jats:p>The core RNA helicase of the EJC, EIF4A3, showed increased expression in atrophied muscles and aging human muscle (+150.43%, <jats:italic>n<\/jats:italic>\u2009=\u20095 in young and aged human, age: 26.20\u2009\u00b1\u20096.760 vs. 73.60\u2009\u00b1\u20095.030, <jats:italic>p<\/jats:italic>\u2009&lt;\u20090.001) and aged mice muscle (+74.54% in male, +61.28% in female: <jats:italic>n<\/jats:italic>\u2009=\u20096 in young and aged mice in male\/female, age: 3\u2009months vs. 20\u2009months, <jats:italic>p<\/jats:italic>\u2009&lt;\u20090.001). In\u00a0vitro studies demonstrated that EIF4A3 overexpression promoted muscle atrophy and aging in myotubes (<jats:italic>n<\/jats:italic>\u2009=\u20096, <jats:italic>p<\/jats:italic>\u2009&lt;\u20090.05), while EIF4A3 inhibition mitigated these effects (<jats:italic>p<\/jats:italic>\u2009&lt;\u20090.05). In\u00a0vivo phenotypic analysis indicated that overexpression of EIF4A3 in skeletal muscle promoted muscle atrophy (<jats:italic>n<\/jats:italic>\u2009=\u200910, <jats:italic>p<\/jats:italic>\u2009&lt;\u20090.05) including reduced grip strength (\u221242.36%, <jats:italic>p<\/jats:italic>\u2009&lt;\u20090.001), running capacity (\u221221.24%, <jats:italic>p<\/jats:italic>\u2009&lt;\u20090.001), contraction force (\u221219.62%, <jats:italic>p<\/jats:italic>\u2009&lt;\u20090.001), muscle weight (gastrocnemius muscle: \u221215.75%; <jats:italic>p<\/jats:italic>\u2009&lt;\u20090.001; tibialis anterior muscle: \u22129.50%, <jats:italic>p<\/jats:italic>\u2009&lt;\u20090.01), myofiber size (\u221211.59%, <jats:italic>p<\/jats:italic>\u2009&lt;\u20090.001) and worsened molecular phenotypes (all <jats:italic>p<\/jats:italic>\u2009&lt;\u20090.05). Knockdown of EIF4A3 protected against muscle atrophy induced by various stimuli, including denervation (<jats:italic>n<\/jats:italic>\u2009=\u200910, <jats:italic>p<\/jats:italic>\u2009&lt;\u20090.05), immobilization (<jats:italic>n<\/jats:italic>\u2009=\u200910, <jats:italic>p<\/jats:italic>\u2009&lt;\u20090.05) and angiotensin II (<jats:italic>n<\/jats:italic>\u2009=\u20096\u201310, <jats:italic>p<\/jats:italic>\u2009&lt;\u20090.05) in mice. Mechanistically, Neural Precursor Cell Expressed, Developmentally Down\u2010Regulated 9 (NEDD9) mRNA was identified as a direct target of EIF4A3. EIF4A3 promoted the decay of NEDD9 mRNA and inhibited the downstream focal adhesion kinase (FAK) and PI3K\u2010Akt pathway, promoting muscle atrophy. Pharmacological activation of the NEDD9\u2010FAK pathway abolished the pro\u2010atrophy effects of EIF4A3.<\/jats:p><\/jats:sec><jats:sec><jats:title>Conclusions<\/jats:title><jats:p>Our findings shed significant light on the pivotal function of the EJC in muscle atrophy, revealing novel mechanisms that contribute to EJC\u2010related disorders. Providing a target for therapeutic interventions aimed at combating muscle atrophy.<\/jats:p><\/jats:sec>","DOI":"10.1002\/jcsm.70010","type":"journal-article","created":{"date-parts":[[2025,7,11]],"date-time":"2025-07-11T06:14:13Z","timestamp":1752214453000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":10,"title":["EIF4A3 Promotes Muscle Atrophy and Aging by Inhibiting the FAK Pathway Through NEDD9 mRNA Destabilization"],"prefix":"10.1002","volume":"16","author":[{"given":"Qian","family":"Li","sequence":"first","affiliation":[{"name":"Cardiac Regeneration and Ageing Lab, Institute of Geriatrics (Shanghai University), Affiliated Nantong Hospital of Shanghai University (The Sixth People's Hospital of Nantong), School of Medicine Shanghai University  Nantong China"},{"name":"Institute of Cardiovascular Sciences, Shanghai Engineering Research Center of Organ Repair, Joint International Research Laboratory of Biomaterials and 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