{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,16]],"date-time":"2026-10-16T18:14:27Z","timestamp":1792174467002,"version":"4.4.0"},"reference-count":58,"publisher":"Wiley","issue":"1","license":[{"start":{"date-parts":[[2026,8,20]],"date-time":"2026-08-20T00:00:00Z","timestamp":1787184000000},"content-version":"vor","delay-in-days":19,"URL":"http:\/\/creativecommons.org\/licenses\/by\/4.0\/"},{"start":{"date-parts":[[2026,8,1]],"date-time":"2026-08-01T00:00:00Z","timestamp":1785542400000},"content-version":"tdm","delay-in-days":0,"URL":"http:\/\/doi.wiley.com\/10.1002\/tdm_license_1.1"}],"funder":[{"DOI":"10.13039\/501100007423","name":"Duchenne Parent Project","doi-asserted-by":"publisher","award":["22.004"],"award-info":[{"award-number":["22.004"]}],"id":[{"id":"10.13039\/501100007423","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100002426","name":"Fondazione Telethon","doi-asserted-by":"publisher","award":["GJC25P084"],"award-info":[{"award-number":["GJC25P084"]}],"id":[{"id":"10.13039\/501100002426","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100021856","name":"Ministero dell'Universit\u00e0 e della Ricerca","doi-asserted-by":"publisher","award":["PRIN MUR 2020ELYA32"],"award-info":[{"award-number":["PRIN MUR 2020ELYA32"]}],"id":[{"id":"10.13039\/501100021856","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["nyaspubs.onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Ann NY Acad Sci"],"published-print":{"date-parts":[[2026,8]]},"abstract":"<jats:title>ABSTRACT<\/jats:title>\n                  <jats:p>\n                    Efficient skeletal muscle contraction requires tight mechano\u2010metabolic coupling, a process regulated by AMP\u2010activated protein kinase (AMPK). Duchenne muscular dystrophy (DMD) is characterized by aberrant AMPK activation and disrupted metabolic signaling. This study investigates the expression and regulation of the LKB1\u2013STRAD\u03b1\u2013MO25 heterotrimeric complex, the primary upstream activator of AMPK, in DMD models. We analyzed muscles from dystrophic mice (BL10\n                    <jats:italic>mdx<\/jats:italic>\n                    and D2\n                    <jats:italic>mdx<\/jats:italic>\n                    ) and patient\u2010derived cells and found significant downregulation of the LKB1 complex across all disease stages in the DMD models, a defect not observed in an amyotrophic lateral sclerosis model. Treatment with the broad\u2010spectrum HDAC inhibitor vorinostat effectively restored LKB1 expression at both transcript and protein levels in D2\n                    <jats:italic>mdx<\/jats:italic>\n                    mice. This restoration was mechanistically linked to downregulation of miR\u2010451, miR\u2010195, and miR\u201017, which function as post\u2010transcriptional repressors of LKB1. Conversely, the selective HDAC1\/2 inhibitor Rodin\u2010A increased\n                    <jats:italic>Lkb1<\/jats:italic>\n                    mRNA but failed to rescue protein levels or alter miRNA expression. Our data identify the axis LKB1\u2013STRAD\u03b1\u2013MO25 as a critical regulatory node that is disrupted in DMD, but remains responsive to epigenetic modulation. These findings suggest that restoring LKB1 activity via HDAC inhibition or miRNA targeting may represent a therapeutic avenue to address dystrophic muscle dysfunction.\n                  <\/jats:p>","DOI":"10.1111\/nyas.70364","type":"journal-article","created":{"date-parts":[[2026,8,20]],"date-time":"2026-08-20T13:15:08Z","timestamp":1787231708000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":1,"title":["LKB1 Dysregulation in Duchenne Muscular Dystrophy Models: Disease Specificity and Epigenetic Control by HDAC Inhibitors"],"prefix":"10.1111","volume":"1562","author":[{"given":"Brigida","family":"Boccanegra","sequence":"first","affiliation":[{"name":"Department of Pharmacy \u2013 Drug Sciences University of Bari \u201cAldo Moro\u201d  Bari Italy"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Lisamaura","family":"Tulimiero","sequence":"additional","affiliation":[{"name":"Department of Pharmacy \u2013 Drug Sciences University of Bari \u201cAldo Moro\u201d  Bari Italy"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Raffaella","family":"Quarta","sequence":"additional","affiliation":[{"name":"Department of Pharmacy \u2013 Drug Sciences University of Bari \u201cAldo Moro\u201d  Bari Italy"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Elena","family":"Conte","sequence":"additional","affiliation":[{"name":"Department of Pharmacy \u2013 Drug Sciences University of Bari \u201cAldo Moro\u201d  Bari Italy"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Simonetta Andrea","family":"Licandro","sequence":"additional","affiliation":[{"name":"Preclinical R&amp;D Department Italfarmaco S.p.A.  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