{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,28]],"date-time":"2026-09-28T20:22:03Z","timestamp":1790626923906,"version":"4.1.0"},"reference-count":60,"publisher":"Frontiers Media SA","license":[{"start":{"date-parts":[[2023,4,12]],"date-time":"2023-04-12T00:00:00Z","timestamp":1681257600000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"content-domain":{"domain":["frontiersin.org"],"crossmark-restriction":true},"short-container-title":["Front. Immunol."],"abstract":"\n Introduction<\/jats:title>\n Growth hormone secretagogues (GHSs) exert multiple actions, being able to activate GHS-receptor 1a, control inflammation and metabolism, to enhance GH\/insulin-like growth factor-1 (IGF-1)-mediated myogenesis, and to inhibit angiotensin-converting enzyme. These mechanisms are of interest for potentially targeting multiple steps of pathogenic cascade in Duchenne muscular dystrophy (DMD).<\/jats:p>\n <\/jats:sec>\n \n Methods<\/jats:title>\n \n Here, we aimed to provide preclinical evidence for potential benefits of GHSs in DMD,\n via<\/jats:italic>\n a multidisciplinary\n in vivo<\/jats:italic>\n and\n ex vivo<\/jats:italic>\n comparison in\n mdx<\/jats:italic>\n mice, of two\n ad hoc<\/jats:italic>\n synthesized compounds (EP80317 and JMV2894), with a wide but different profile. 4-week-old\n mdx<\/jats:italic>\n mice were treated for 8 weeks with EP80317 or JMV2894 (320 \u00b5g\/kg\/d, s.c.).\n <\/jats:p>\n <\/jats:sec>\n \n Results<\/jats:title>\n \n In vivo<\/jats:italic>\n , both GHSs increased mice forelimb force (recovery score, RS towards WT: 20% for EP80317 and 32% for JMV2894 at week 8). In parallel, GHSs also reduced diaphragm (DIA) and gastrocnemius (GC) ultrasound echodensity, a fibrosis-related parameter (RS: ranging between 26% and 75%).\n Ex vivo<\/jats:italic>\n , both drugs ameliorated DIA isometric force and calcium-related indices (\n e.g.<\/jats:italic>\n , RS: 40% for tetanic force). Histological analysis highlighted a relevant reduction of fibrosis in GC and DIA muscles of treated mice, paralleled by a decrease in gene expression of\n TGF-\u03b21<\/jats:italic>\n and\n Col1a1<\/jats:italic>\n . Also, decreased levels of pro-inflammatory genes (\n IL-6, CD68<\/jats:italic>\n ), accompanied by an increment in\n Sirt-1, PGC-1\u03b1<\/jats:italic>\n and\n MEF2c<\/jats:italic>\n expression, were observed in response to treatments, suggesting an overall improvement of myofiber metabolism. No detectable transcript levels of\n GHS receptor-1a<\/jats:italic>\n , nor an increase of circulating IGF-1 were found, suggesting the presence of a novel receptor-independent mechanism in skeletal muscle. Preliminary docking studies revealed a potential binding capability of JMV2894 on metalloproteases involved in extracellular matrix remodeling and cytokine production, such as ADAMTS-5 and MMP-9, overactivated in DMD.\n <\/jats:p>\n <\/jats:sec>\n \n Discussion<\/jats:title>\n \n Our results support the interest of GHSs as modulators of pathology progression in\n mdx<\/jats:italic>\n mice, disclosing a direct anti-fibrotic action that may prove beneficial to contrast pathological remodeling.\n <\/jats:p>\n <\/jats:sec>","DOI":"10.3389\/fimmu.2023.1119888","type":"journal-article","created":{"date-parts":[[2023,4,12]],"date-time":"2023-04-12T00:29:42Z","timestamp":1681259382000},"update-policy":"https:\/\/doi.org\/10.3389\/crossmark-policy","source":"Crossref","is-referenced-by-count":23,"title":["Growth hormone secretagogues modulate inflammation and fibrosis in mdx mouse model of Duchenne muscular 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