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Study · Animal study (in vivo) · 2023

6 results

The mitochondrially targeted peptide elamipretide (SS-31) improves ADP sensitivity in aged mitochondria by increasing uptake through the adenine nucleotide translocator (ANT).

Pharaoh G, Kamat V, Kannan S, Stuppard RS, Whitson J, Martín-Pérez M, Qian WJ, MacCoss MJ, Villén J, Rabinovitch P, Campbell MD, Sweet IR, Marcinek DJ

GeroScience18 Jul 2023Cited by 42 (Europe PMC)

PMID37462785 (opens in a new tab)PMCIDPMC10643647 (opens in a new tab)DOI10.1007/s11357-023-00861-y (opens in a new tab)PepBankPUB-37462785
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Summary

Aging muscle experiences functional decline in part mediated by impaired mitochondrial ADP sensitivity. Elamipretide (ELAM) rapidly improves physiological and mitochondrial function in aging and binds directly to the mitochondrial ADP transporter ANT. We hypothesized that ELAM improves ADP sensitivity in aging leading to rescued physiological function. We measured the response to ADP stimulation in young and old muscle mitochondria with ELAM treatment, in vivo heart and muscle function, and compared protein abundance, phosphorylation, and S-glutathionylation of ADP/ATP pathway proteins. ELAM treatment increased ADP sensitivity in old muscle mitochondria by increasing uptake of ADP through the ANT and rescued muscle force and heart systolic function. Protein abundance in the ADP/ATP transport and synthesis pathway was unchanged, but ELAM treatment decreased protein s-glutathionylation incuding of ANT. Mitochondrial ADP sensitivity is rapidly modifiable. This research supports the hypothesis that ELAM improves ANT function in aging and links mitochondrial ADP sensitivity to physiological function. ELAM binds directly to ANT and ATP synthase and ELAM treatment improves ADP sensitivity, increases ATP production, and improves physiological function in old muscles. ADP (adenosine diphosphate), ATP (adenosine triphosphate), VDAC (voltage-dependent anion channel), ANT (adenine nucleotide translocator), H+ (proton), ROS (reactive oxygen species), NADH (nicotinamide adenine dinucleotide), FADH2 (flavin adenine dinucleotide), O2 (oxygen), ELAM (elamipretide), -SH (free thiol), -SSG (glutathionylated protein).
CC BYText from Europe PMC. Highlighted sentences are the source of results.

Results from this study6

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

  1. 01AnimalAnimal study (in vivo)Efficacy outcome

    In old animals, elamipretide rescued muscle force.

    In plain wordsIn old animals, elamipretide restored muscle force.

    Peptide
    Elamipretide (SS-31)
    Outcome
    IncreaseMuscle force in old animals
    Study

    n: not reported in source

    Outcome group
    Exercise and physical function · Musculoskeletal
    Studied dose
    Dose not stated

    Source sentences

    Summary
    ELAM treatment increased ADP sensitivity in old muscle mitochondria by increasing uptake of ADP through the ANT and rescued muscle force and heart systolic function.
    1 context sentence
    Summary · context
    We measured the response to ADP stimulation in young and old muscle mitochondria with ELAM treatment, in vivo heart and muscle function, and compared protein abundance, phosphorylation, and S-glutathionylation of ADP/ATP pathway proteins.
  2. 02AnimalAnimal study (in vivo)Efficacy outcome

    In old animals, elamipretide rescued heart systolic function.

    In plain wordsIn old animals, elamipretide restored heart pumping function.

    Peptide
    Elamipretide (SS-31)
    Outcome
    IncreaseHeart systolic function in old animals
    Study

    n: not reported in source

    Outcome group
    Heart function · Cardiovascular
    Studied dose
    Dose not stated

    Source sentences

    Summary
    ELAM treatment increased ADP sensitivity in old muscle mitochondria by increasing uptake of ADP through the ANT and rescued muscle force and heart systolic function.
    1 context sentence
    Summary · context
    We measured the response to ADP stimulation in young and old muscle mitochondria with ELAM treatment, in vivo heart and muscle function, and compared protein abundance, phosphorylation, and S-glutathionylation of ADP/ATP pathway proteins.
  3. 03LabEx vivo tissueMechanism

    In old muscle mitochondria, elamipretide increased ADP sensitivity.

    In plain wordsIn lab tests of old muscle mitochondria, elamipretide improved how well they responded to ADP.

    Peptide
    Elamipretide (SS-31)
    Outcome
    IncreaseADP sensitivity in old muscle mitochondria
    Study

    n: not reported in source

    Young and old muscle mitochondria
    Outcome group
    Mitochondrial function · Aging and longevity
    Studied dose
    Dose not stated

    Source sentences

    Summary
    ELAM treatment increased ADP sensitivity in old muscle mitochondria by increasing uptake of ADP through the ANT and rescued muscle force and heart systolic function.
    1 context sentence
    Summary · context
    We measured the response to ADP stimulation in young and old muscle mitochondria with ELAM treatment, in vivo heart and muscle function, and compared protein abundance, phosphorylation, and S-glutathionylation of ADP/ATP pathway proteins.
  4. 04LabEx vivo tissueMechanism

    In old muscle mitochondria, elamipretide increased ADP uptake through the adenine nucleotide translocator.

    In plain wordsIn lab tests of old muscle mitochondria, elamipretide increased ADP uptake through the ANT transporter.

    Peptide
    Elamipretide (SS-31)
    Outcome
    IncreaseADP uptake through ANT
    Study

    n: not reported in source

    Old muscle mitochondria
    Outcome group
    Mitochondrial function · Aging and longevity
    Studied dose
    Dose not stated

    Source sentences

    Summary
    ELAM treatment increased ADP sensitivity in old muscle mitochondria by increasing uptake of ADP through the ANT and rescued muscle force and heart systolic function.
    1 context sentence
    Summary · context
    We measured the response to ADP stimulation in young and old muscle mitochondria with ELAM treatment, in vivo heart and muscle function, and compared protein abundance, phosphorylation, and S-glutathionylation of ADP/ATP pathway proteins.
  5. 05LabEx vivo tissueMechanism

    In muscle mitochondria, elamipretide did not change protein abundance in the ADP/ATP transport and synthesis pathway.

    In plain wordsIn lab tests, elamipretide did not change the amount of ADP/ATP pathway proteins.

    Peptide
    Elamipretide (SS-31)
    Outcome
    No significant changeADP/ATP pathway protein abundance
    Study

    n: not reported in source

    Muscle mitochondria
    Outcome group
    Mitochondrial function · Aging and longevity
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Protein abundance in the ADP/ATP transport and synthesis pathway was unchanged
    1 context sentence
    Summary · context
    We measured the response to ADP stimulation in young and old muscle mitochondria with ELAM treatment, in vivo heart and muscle function, and compared protein abundance, phosphorylation, and S-glutathionylation of ADP/ATP pathway proteins.
  6. 06LabEx vivo tissueMechanism

    In muscle mitochondria, elamipretide decreased protein S-glutathionylation, including that of ANT.

    In plain wordsIn lab tests, elamipretide lowered a chemical change on proteins, including the ANT transporter.

    Peptide
    Elamipretide (SS-31)
    Outcome
    DecreaseProtein S-glutathionylation including ANT
    Study

    n: not reported in source

    Muscle mitochondria
    Outcome group
    Mitochondrial function · Aging and longevity
    Studied dose
    Dose not stated

    Source sentences

    Summary
    but ELAM treatment decreased protein s-glutathionylation incuding of ANT.
    1 context sentence
    Summary · context
    We measured the response to ADP stimulation in young and old muscle mitochondria with ELAM treatment, in vivo heart and muscle function, and compared protein abundance, phosphorylation, and S-glutathionylation of ADP/ATP pathway proteins.

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

    10 Oct 2026, 08:19 UTC

    Study results updated

  2. Version 1

    9 Oct 2026, 02:47 UTC

    First added · source update from Europe PMC

Subjects

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