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Study · Not a test of the peptide alone · 2025

1 result

Telomere length in offspring is determined by mitochondrial-nuclear communication at fertilization.

Winstanley YE, Rose RD, Sobinoff AP, Wu LL, Adhikari D, Zhang QH, Wells JK, Wong LH, Szeto HH, Piltz SG, Thomas PQ, Febbraio MA and 4 more

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Carroll J, Pickett HA, Russell DL, Robker RL

Nature communications14 Mar 2025Cited by 11 (Europe PMC)

Summary

The initial setting of telomere length during early life in each individual has a major influence on lifetime risk of aging-associated diseases; however there is limited knowledge of biological signals that regulate inheritance of telomere length, and whether it is modifiable is not known. We now show that when mitochondrial activity is disrupted in mouse zygotes, via exposure to 20% O2 or rotenone, telomere elongation between the 8-cell and blastocyst stage is impaired, with shorter telomeres apparent in the pluripotent Inner Cell Mass (ICM) and persisting after organogenesis. Identical defects of elevated mtROS in zygotes followed by impaired telomere elongation, occurred with maternal obesity or advanced age. We further demonstrate that telomere elongation during ICM formation is controlled by mitochondrial-nuclear communication at fertilization. Using mitochondrially-targeted therapeutics (BGP-15, MitoQ, SS-31, metformin) we demonstrate that it is possible to modulate the preimplantation telomere resetting process and restore deficiencies in neonatal telomere length.
CC BYText from Europe PMC. Highlighted sentences are the source of results.

Results from this study1

No result from this study comes from a test of the peptide.

Studies that did not test the peptide alone1

In this study, Elamipretide (SS-31) was a lab tool or a carrier, part of a mix, or the subject of a lab method. These results are not evidence about taking Elamipretide (SS-31).

  1. 01AnimalNot a test of Elamipretide (SS-31) aloneAnimal study (in vivo)Efficacy outcome

    In mouse embryos with disrupted mitochondrial activity, pooled mitochondrially-targeted agents (BGP-15, MitoQ, SS‑31, metformin) restored deficiencies in neonatal telomere length.

    In plain wordsIn mice, a group of mitochondria-targeted agents that included SS‑31 restored shorter newborn telomere length.

    Outcome
    IncreaseNeonatal telomere length restoration
    Study

    mousen: not reported in source

    mouse zygotes and preimplantation embryos
    Outcome group
    Aging markers · Aging and longevity

    Source sentences

    Summary
    Using mitochondrially-targeted therapeutics (BGP-15, MitoQ, SS-31, metformin) we demonstrate that it is possible to modulate the preimplantation telomere resetting process and restore deficiencies in neonatal telomere length.
    1 context sentence
    Summary · context
    We now show that when mitochondrial activity is disrupted in mouse zygotes, via exposure to 20% O2 or rotenone, telomere elongation between the 8-cell and blastocyst stage is impaired, with shorter telomeres apparent in the pluripotent Inner Cell Mass (ICM) and persisting after organogenesis.

    In this study, Elamipretide (SS-31) was a lab tool or a carrier, part of a mix, or the subject of a lab method. This result is not evidence about taking Elamipretide (SS-31).

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

Terms as the source lists them.

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