Humanin improves bone health in a glucocorticoid-treated mouse model of Duchenne muscular dystrophy.

Cedervall T, Jude B, von Walden F, Velentza L, Lanner JT, Sejersen T, Zaman F, Sävendahl L

Biochemistry and biophysics reports6 Jan 2026

PMID41550496PMCIDPMC12811480DOI10.1016/j.bbrep.2025.102421PepBankPUB-41550496

Summary

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 ex vivo force measurements. D2.mdx, but not B10.mdx, showed decreased bone growth and impaired bone structure compared with wild type (WT). D2.mdx also displayed increased growth plate height with lower endogenous humanin expression than D2.WT. GC treatment caused growth retardation and reductions in cortical bone area, thickness, and mineral content. Co-administration with HNG prevented bone growth impairment at one week of treatment and mitigated GC adverse effects on cortical bone in B10.mdx mice. Adding HNG to GCs did not exacerbate skeletal muscle pathology; in fact, HNG had a mild enlarging effect on muscle fibers. These data suggest that HNG is a potential candidate for improving bone health in DMD during GC therapy. Further in vivo studies are needed to determine optimal HNG dosing and to assess the effects of long-term treatment on skeletal muscle function.

CC BYText from Europe PMC. Highlighted sentences are the source of results.

Results from this study5

4 results from studies that gave the peptide. No result from this study comes from people.

01AnimalAnimal study (in vivo)Efficacy outcome
In B10.mdx mice, co-administration of HNG with glucocorticoids prevented bone growth impairment at one week of treatment.
In plain wordsIn mice, adding HNG to glucocorticoids prevented the early slowing of bone growth that glucocorticoids caused.
Peptide
Humanin
Outcome
IncreaseBone growth impairment at one week of glucocorticoid treatment
Study
mousen: not reported in source
B10.mdx mice treated with glucocorticoids
Comparator
Glucocorticoids without HNG
Outcome group
Bone and joint · Musculoskeletal
Studied dose
Dose not stated · from 5 to 9 weeks of ageAs given in this study (mouse).
Source sentences
Summary
Co-administration with HNG prevented bone growth impairment at one week of treatment
2 context sentences(design, population, supporting numbers)
Summary · context
GC treatment caused growth retardation and reductions in cortical bone area, thickness, and mineral content.
Summary · context
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.
Show in the study text Report a problemFND-4155049602
02AnimalAnimal study (in vivo)Efficacy outcome
In B10.mdx mice, co-administration of HNG mitigated glucocorticoid adverse effects on cortical bone.
In plain wordsIn mice, adding HNG to glucocorticoids reduced the harm that glucocorticoids did to the outer layer of bone.
Peptide
Humanin
Outcome
IncreaseCortical bone adverse effects of glucocorticoids
Study
mousen: not reported in source
B10.mdx mice treated with glucocorticoids
Comparator
Glucocorticoids without HNG
Outcome group
Bone and joint · Musculoskeletal
Studied dose
Dose not stated · from 5 to 9 weeks of ageAs given in this study (mouse).
Source sentences
Summary
mitigated GC adverse effects on cortical bone in B10.mdx mice.
2 context sentences(design, population, supporting numbers)
Summary · context
GC treatment caused growth retardation and reductions in cortical bone area, thickness, and mineral content.
Summary · context
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.
Show in the study text Report a problemFND-4155049603
03AnimalAnimal study (in vivo)Safety outcome
Adding HNG to glucocorticoids did not exacerbate skeletal muscle pathology in mdx mice.
In plain wordsIn mice, adding HNG to glucocorticoids did not make muscle damage worse.
Peptide
Humanin
Outcome
No significant changeSkeletal muscle pathology when HNG was added to glucocorticoids
Study
mousen: not reported in source
B10.mdx and D2.mdx mouse models of Duchenne muscular dystrophy
Comparator
Glucocorticoids without HNG
Outcome group
Muscle injury and repair · Musculoskeletal
Studied dose
Dose not stated · from 5 to 9 weeks of ageAs given in this study (mouse).
Source sentences
Summary
Adding HNG to GCs did not exacerbate skeletal muscle pathology
1 context sentence(design, population, supporting numbers)
Summary · context
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.
Show in the study text Report a problemFND-4155049604
04AnimalAnimal study (in vivo)Efficacy outcome
In mdx mice, HNG had a mild enlarging effect on muscle fibers.
In plain wordsIn mice, HNG slightly enlarged muscle fibers.
Peptide
Humanin
Outcome
IncreaseMuscle fiber size with HNG
Study
mousen: not reported in source
B10.mdx and D2.mdx mouse models of Duchenne muscular dystrophy
Comparator
Glucocorticoids without HNG
Outcome group
Muscle injury and repair · Musculoskeletal
Studied dose
Dose not stated · from 5 to 9 weeks of ageAs given in this study (mouse).
Source sentences
Summary
HNG had a mild enlarging effect on muscle fibers.
1 context sentence(design, population, supporting numbers)
Summary · context
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.
Show in the study text Report a problemFND-4155049605

Natural levels measured1

These results measure the body's own peptide. Nobody was given the peptide. They are not evidence about taking it. They are left out of key results, evidence counts and charts.

05AnimalEndogenous levelAnimal study (in vivo)Efficacy outcome
D2.mdx mice showed lower endogenous humanin expression than D2.WT mice.
In plain wordsIn mice, D2.mdx mice had lower natural humanin expression than normal D2 mice.
Peptide
Humanin
Outcome
DecreaseEndogenous humanin expression in D2.mdx versus D2.WT mice
Study
mousen: not reported in source
D2.mdx and D2.WT mice
Comparator
D2.WT mice
Outcome group
Aging markers · Musculoskeletal
Source sentences
Summary
with lower endogenous humanin expression than D2.WT.
1 context sentence(design, population, supporting numbers)
Summary · context
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.
This result measures the body's own Humanin. Nobody was given the peptide. It is not evidence about taking it.
Show in the study text Report a problemFND-4155049601

AI wrote and checked these results. AI can make mistakes, so check important results against the source.

Version history

PepBank keeps every version of the data on this study. Status changes from Retraction Watch, Europe PMC and Crossref are listed with their source.

Version 2Current
13 Oct 2026, 21:44 UTC
Study results updated
Version 1
13 Oct 2026, 16:31 UTC
First added · source update from Europe PMC

Subjects

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