Skip to content

Study · Animal study (in vivo) · mouse (c57bl and 6j) · 2025

9 results

The Mitochondria-Targeted Peptide Therapeutic Elamipretide Improves Cardiac and Skeletal Muscle Function During Aging Without Detectable Changes in Tissue Epigenetic or Transcriptomic Age.

Mitchell W, Pharaoh G, Tyshkovskiy A, Campbell M, Marcinek DJ, Gladyshev VN

Aging cell13 Mar 2025Cited by 21 (Europe PMC)

PMID40080911 (opens in a new tab)PMCIDPMC12151887 (opens in a new tab)DOI10.1111/acel.70026 (opens in a new tab)PepBankPUB-40080911
Download PDFPubMedAsk about this study
Jump to 9 results

Summary

Aging-related decreases in cardiac and skeletal muscle function are strongly associated with various comorbidities. Elamipretide (ELAM), a novel mitochondria-targeted peptide, has demonstrated broad therapeutic efficacy in ameliorating disease conditions associated with mitochondrial dysfunction across both clinical and pre-clinical models. Herein, we investigated the impact of 8-week ELAM treatment on pre- and post-measures of C57BL/6J mice frailty, skeletal muscle, and cardiac muscle function, coupled with post-treatment assessments of biological age and affected molecular pathways. We found that health status, as measured by frailty index, cardiac strain, diastolic function, and skeletal muscle force, is significantly diminished with age, with skeletal muscle force changing in a sex-dependent manner. Conversely, ELAM mitigated frailty accumulation and was able to partially reverse these declines, as evidenced by treatment-induced increases in cardiac strain and muscle fatigue resistance. Despite these improvements, we did not detect statistically significant changes in gene expression or DNA methylation profiles indicative of molecular reorganization or reduced biological age in most ELAM-treated groups. However, pathway analyses revealed that ELAM treatment showed pro-longevity shifts in gene expression, such as upregulation of genes involved in fatty acid metabolism, mitochondrial translation, and oxidative phosphorylation, and downregulation of inflammation. Together, these results indicate that ELAM treatment is effective at mitigating signs of sarcopenia and cardiac dysfunction in an aging mouse model, but that these functional improvements occur independently of detectable changes in epigenetic and transcriptomic age. Thus, some age-related changes in function may be uncoupled from changes in molecular biological age.
CC BYText from Europe PMC. Highlighted sentences are the source of results.

Results from this study9

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

  1. 01AnimalAnimal study (in vivo)Efficacy outcome

    In aging C57BL/6J mice, 8 weeks of elamipretide mitigated frailty accumulation.

    In plain wordsIn aging mice, elamipretide slowed the build-up of frailty.

    Peptide
    Elamipretide (SS-31)
    Outcome
    DecreaseFrailty accumulation
    Study

    mouse (C57BL/6J)n: not reported in source

    Aging mouse model
    Outcome group
    Aging markers · Aging and longevity
    Studied dose
    Dose not stated · 8 weeksAs given in this study (mouse (C57BL/6J)).

    Source sentences

    Summary
    Conversely, ELAM mitigated frailty accumulation and was able to partially reverse these declines, as evidenced by treatment-induced increases in cardiac strain and muscle fatigue resistance.
    1 context sentence
    Summary · context
    Herein, we investigated the impact of 8-week ELAM treatment on pre- and post-measures of C57BL/6J mice frailty, skeletal muscle, and cardiac muscle function, coupled with post-treatment assessments of biological age and affected molecular pathways.
  2. 02AnimalAnimal study (in vivo)Efficacy outcome

    In aging C57BL/6J mice, elamipretide treatment increased cardiac strain, partially reversing the age-related decline.

    In plain wordsIn aging mice, elamipretide improved heart strain, partly reversing an age-related decline.

    Peptide
    Elamipretide (SS-31)
    Outcome
    IncreaseCardiac strain
    Study

    mouse (C57BL/6J)n: not reported in source

    Aging mouse model
    Outcome group
    Heart function · Cardiovascular
    Studied dose
    Dose not stated · 8 weeksAs given in this study (mouse (C57BL/6J)).

    Source sentences

    Summary
    Conversely, ELAM mitigated frailty accumulation and was able to partially reverse these declines, as evidenced by treatment-induced increases in cardiac strain and muscle fatigue resistance.
    1 context sentence
    Summary · context
    Herein, we investigated the impact of 8-week ELAM treatment on pre- and post-measures of C57BL/6J mice frailty, skeletal muscle, and cardiac muscle function, coupled with post-treatment assessments of biological age and affected molecular pathways.
  3. 03AnimalAnimal study (in vivo)Efficacy outcome

    In aging C57BL/6J mice, elamipretide treatment increased muscle fatigue resistance, partially reversing the age-related decline.

    In plain wordsIn aging mice, elamipretide improved muscle fatigue resistance, partly reversing an age-related decline.

    Peptide
    Elamipretide (SS-31)
    Outcome
    IncreaseSkeletal muscle fatigue resistance
    Study

    mouse (C57BL/6J)n: not reported in source

    Aging mouse model
    Outcome group
    Exercise and physical function · Musculoskeletal
    Studied dose
    Dose not stated · 8 weeksAs given in this study (mouse (C57BL/6J)).

    Source sentences

    Summary
    Conversely, ELAM mitigated frailty accumulation and was able to partially reverse these declines, as evidenced by treatment-induced increases in cardiac strain and muscle fatigue resistance.
    1 context sentence
    Summary · context
    Herein, we investigated the impact of 8-week ELAM treatment on pre- and post-measures of C57BL/6J mice frailty, skeletal muscle, and cardiac muscle function, coupled with post-treatment assessments of biological age and affected molecular pathways.
  4. 04AnimalAnimal study (in vivo)Mechanism

    In aging C57BL/6J mice, elamipretide produced no statistically significant change in gene expression profiles indicating reduced biological age in most treated groups.

    In plain wordsIn aging mice, elamipretide did not significantly change gene activity patterns linked to biological age in most treated groups.

    Peptide
    Elamipretide (SS-31)
    Outcome
    No significant changeGene expression profile (biological age)
    Study

    mouse (C57BL/6J)n: not reported in source

    Aging mouse model
    Outcome group
    Aging markers · Aging and longevity
    Studied dose
    Dose not stated · 8 weeksAs given in this study (mouse (C57BL/6J)).

    Source sentences

    Summary
    we did not detect statistically significant changes in gene expression
    1 context sentence
    Summary · context
    Herein, we investigated the impact of 8-week ELAM treatment on pre- and post-measures of C57BL/6J mice frailty, skeletal muscle, and cardiac muscle function, coupled with post-treatment assessments of biological age and affected molecular pathways.
  5. 05AnimalAnimal study (in vivo)Mechanism

    In aging C57BL/6J mice, elamipretide produced no statistically significant change in DNA methylation profiles indicating reduced biological age in most treated groups.

    In plain wordsIn aging mice, elamipretide did not significantly change DNA methylation patterns linked to biological age in most treated groups.

    Peptide
    Elamipretide (SS-31)
    Outcome
    No significant changeDNA methylation profile (epigenetic age)
    Study

    mouse (C57BL/6J)n: not reported in source

    Aging mouse model
    Outcome group
    Aging markers · Aging and longevity
    Studied dose
    Dose not stated · 8 weeksAs given in this study (mouse (C57BL/6J)).

    Source sentences

    Summary
    Despite these improvements, we did not detect statistically significant changes in gene expression or DNA methylation profiles indicative of molecular reorganization or reduced biological age in most ELAM-treated groups.
    1 context sentence
    Summary · context
    Herein, we investigated the impact of 8-week ELAM treatment on pre- and post-measures of C57BL/6J mice frailty, skeletal muscle, and cardiac muscle function, coupled with post-treatment assessments of biological age and affected molecular pathways.
  6. 06AnimalAnimal study (in vivo)Mechanism

    In aging C57BL/6J mice, pathway analysis showed elamipretide upregulated genes involved in fatty acid metabolism.

    In plain wordsIn aging mice, elamipretide turned up genes for fatty acid metabolism.

    Peptide
    Elamipretide (SS-31)
    Outcome
    IncreaseFatty acid metabolism gene expression
    Study

    mouse (C57BL/6J)n: not reported in source

    Aging mouse model
    Outcome group
    Mitochondrial function · Metabolic and weight
    Studied dose
    Dose not stated · 8 weeksAs given in this study (mouse (C57BL/6J)).

    Source sentences

    Summary
    upregulation of genes involved in fatty acid metabolism, mitochondrial translation, and oxidative phosphorylation
    1 context sentence
    Summary · context
    Herein, we investigated the impact of 8-week ELAM treatment on pre- and post-measures of C57BL/6J mice frailty, skeletal muscle, and cardiac muscle function, coupled with post-treatment assessments of biological age and affected molecular pathways.
  7. 07AnimalAnimal study (in vivo)Mechanism

    In aging C57BL/6J mice, pathway analysis showed elamipretide upregulated genes involved in mitochondrial translation.

    In plain wordsIn aging mice, elamipretide turned up genes for mitochondrial protein production.

    Peptide
    Elamipretide (SS-31)
    Outcome
    IncreaseMitochondrial translation gene expression
    Study

    mouse (C57BL/6J)n: not reported in source

    Aging mouse model
    Outcome group
    Mitochondrial function · Aging and longevity
    Studied dose
    Dose not stated · 8 weeksAs given in this study (mouse (C57BL/6J)).

    Source sentences

    Summary
    upregulation of genes involved in fatty acid metabolism, mitochondrial translation, and oxidative phosphorylation
    1 context sentence
    Summary · context
    Herein, we investigated the impact of 8-week ELAM treatment on pre- and post-measures of C57BL/6J mice frailty, skeletal muscle, and cardiac muscle function, coupled with post-treatment assessments of biological age and affected molecular pathways.
  8. 08AnimalAnimal study (in vivo)Mechanism

    In aging C57BL/6J mice, pathway analysis showed elamipretide upregulated genes involved in oxidative phosphorylation.

    In plain wordsIn aging mice, elamipretide turned up genes for mitochondrial energy production.

    Peptide
    Elamipretide (SS-31)
    Outcome
    IncreaseOxidative phosphorylation gene expression
    Study

    mouse (C57BL/6J)n: not reported in source

    Aging mouse model
    Outcome group
    Mitochondrial function · Aging and longevity
    Studied dose
    Dose not stated · 8 weeksAs given in this study (mouse (C57BL/6J)).

    Source sentences

    Summary
    upregulation of genes involved in fatty acid metabolism, mitochondrial translation, and oxidative phosphorylation
    1 context sentence
    Summary · context
    Herein, we investigated the impact of 8-week ELAM treatment on pre- and post-measures of C57BL/6J mice frailty, skeletal muscle, and cardiac muscle function, coupled with post-treatment assessments of biological age and affected molecular pathways.
  9. 09AnimalAnimal study (in vivo)Mechanism

    In aging C57BL/6J mice, pathway analysis showed elamipretide downregulated inflammation-related gene expression.

    In plain wordsIn aging mice, elamipretide turned down genes linked to inflammation.

    Peptide
    Elamipretide (SS-31)
    Outcome
    DecreaseInflammation gene expression
    Study

    mouse (C57BL/6J)n: not reported in source

    Aging mouse model
    Outcome group
    Inflammation markers · Immune and inflammation
    Studied dose
    Dose not stated · 8 weeksAs given in this study (mouse (C57BL/6J)).

    Source sentences

    Summary
    downregulation of inflammation.
    1 context sentence
    Summary · context
    Herein, we investigated the impact of 8-week ELAM treatment on pre- and post-measures of C57BL/6J mice frailty, skeletal muscle, and cardiac muscle function, coupled with post-treatment assessments of biological age and affected molecular pathways.

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.

  1. Version 2Current

    9 Oct 2026, 18:17 UTC

    Study results updated

  2. Version 1

    9 Oct 2026, 02:47 UTC

    First added · source update from Europe PMC

Subjects

Terms as the source lists them.

PepBank is a research reference. Talk to a doctor before you use any peptide.