ArticleBiochemistry and biophysics reports2026
Humanin improves bone health in a glucocorticoid-treated mouse model of Duchenne muscular dystrophy.
Article in Biochemistry and biophysics reports, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Duchenne muscular dystrophy (DMD) is a progressive muscle disease for which glucocorticoid (GC) treatment is standard therapy. Patients typically suffer from short stature and osteoporosis, caused by the underlying disease and adverse effects of GCs. We investigated whether the mitochondrial peptide humanin (HNG) could prevent GC-induced growth retardation and osteoporosis in mouse models of DMD. Male mdx mice (B10.mdx and D2.mdx) were treated with GCs, with/without HNG, from 5 to 9 weeks of age using two different treatment regimens. Tibial growth was monitored by weekly X-ray imaging; growth plates analyzed with immunohistochemistry and histomorphometry; and bone structure examined using peripheral quantitative computed tomography. Effects on skeletal muscle were evaluated by immunohistochemistry, qPCR, and
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