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Study · In vitro (cells) · 2018

8 results

Mitochondrial peptides modulate mitochondrial function during cellular senescence.

Kim SJ, Mehta HH, Wan J, Kuehnemann C, Chen J, Hu JF, Hoffman AR, Cohen P

Aging1 Jun 2018Cited by 122 (Europe PMC)

PMID29886458 (opens in a new tab)PMCIDPMC6046248 (opens in a new tab)DOI10.18632/aging.101463 (opens in a new tab)PepBankPUB-29886458
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Summary

Cellular senescence is a complex cell fate response that is thought to underlie several age-related pathologies. Despite a loss of proliferative potential, senescent cells are metabolically active and produce energy-consuming effectors, including senescence-associated secretory phenotypes (SASPs). Mitochondria play crucial roles in energy production and cellular signaling, but the key features of mitochondrial physiology and particularly of mitochondria-derived peptides (MDPs), remain underexplored in senescence responses. Here, we used primary human fibroblasts made senescent by replicative exhaustion, doxorubicin or hydrogen peroxide treatment, and examined the number of mitochondria and the levels of mitochondrial respiration, mitochondrial DNA methylation and the mitochondria-encoded peptides humanin, MOTS-c, SHLP2 and SHLP6. Senescent cells showed increased numbers of mitochondria and higher levels of mitochondrial respiration, variable changes in mitochondrial DNA methylation, and elevated levels of humanin and MOTS-c. Humanin and MOTS-c administration modestly increased mitochondrial respiration and selected components of the SASP in doxorubicin-induced senescent cells partially via JAK pathway. Targeting metabolism in senescence cells is an important strategy to reduce SASP production for eliminating the deleterious effects of senescence. These results provide insight into the role of MDPs in mitochondrial energetics and the production of SASP components by senescent cells.
CC BYText from Europe PMC. Highlighted sentences are the source of results.

Results from this study8

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

  1. 01LabIn vitro (cells)Efficacy outcome

    In doxorubicin-induced senescent fibroblasts, MOTS‑c administration modestly increased mitochondrial respiration.

    In plain wordsIn lab-grown human cells, MOTS‑c modestly increased mitochondrial respiration in aged cells.

    Peptide
    MOTS-c
    Outcome
    IncreaseMitochondrial respiration after MOTS-c
    Study

    humann: not reported in source

    primary human fibroblasts made senescent
    Outcome group
    Mitochondrial function · Aging and longevity
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Humanin and MOTS-c administration modestly increased mitochondrial respiration and selected components of the SASP in doxorubicin-induced senescent cells partially via JAK pathway.
    1 context sentence
    Summary · context
    Here, we used primary human fibroblasts made senescent by replicative exhaustion, doxorubicin or hydrogen peroxide treatment, and examined the number of mitochondria and the levels of mitochondrial respiration, mitochondrial DNA methylation and the mitochondria-encoded peptides humanin, MOTS-c, SHLP2 and SHLP6.
  2. 02LabIn vitro (cells)Efficacy outcome

    In doxorubicin-induced senescent fibroblasts, MOTS‑c administration modestly increased selected components of the senescence-associated secretory phenotype.

    In plain wordsIn lab-grown human cells, MOTS‑c modestly increased some secreted inflammatory factors of aged cells.

    Peptide
    MOTS-c
    Outcome
    IncreaseSASP components after MOTS-c
    Study

    humann: not reported in source

    primary human fibroblasts made senescent
    Outcome group
    Inflammation markers · Immune and inflammation
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Humanin and MOTS-c administration modestly increased mitochondrial respiration and selected components of the SASP in doxorubicin-induced senescent cells partially via JAK pathway.
    1 context sentence
    Summary · context
    Here, we used primary human fibroblasts made senescent by replicative exhaustion, doxorubicin or hydrogen peroxide treatment, and examined the number of mitochondria and the levels of mitochondrial respiration, mitochondrial DNA methylation and the mitochondria-encoded peptides humanin, MOTS-c, SHLP2 and SHLP6.
  3. 03LabIn vitro (cells)Mechanism

    In doxorubicin-induced senescent fibroblasts, the effects of MOTS‑c on respiration and SASP components occurred partially via the JAK pathway.

    In plain wordsIn lab-grown human cells, the effects of MOTS‑c partly depended on the JAK pathway.

    Peptide
    MOTS-c
    Outcome
    Not applicableJAK pathway involvement
    Study

    humann: not reported in source

    primary human fibroblasts made senescent
    Outcome group
    Receptor activity and mechanism · Aging and longevity
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Humanin and MOTS-c administration modestly increased mitochondrial respiration and selected components of the SASP in doxorubicin-induced senescent cells partially via JAK pathway.
    1 context sentence
    Summary · context
    Here, we used primary human fibroblasts made senescent by replicative exhaustion, doxorubicin or hydrogen peroxide treatment, and examined the number of mitochondria and the levels of mitochondrial respiration, mitochondrial DNA methylation and the mitochondria-encoded peptides humanin, MOTS-c, SHLP2 and SHLP6.
  4. 04LabIn vitro (cells)Efficacy outcome

    In doxorubicin-induced senescent human fibroblasts, humanin and MOTS-c administration modestly increased mitochondrial respiration.

    In plain wordsIn lab tests on senescent human cells, humanin and MOTS-c modestly increased mitochondrial respiration.

    Peptide
    Humanin
    Outcome
    IncreaseMitochondrial respiration after humanin and MOTS-c
    Study

    humann: not reported in source

    primary human fibroblasts made senescent
    Outcome group
    Mitochondrial function · Aging and longevity
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Humanin and MOTS-c administration modestly increased mitochondrial respiration and selected components of the SASP in doxorubicin-induced senescent cells partially via JAK pathway.
    1 context sentence
    Summary · context
    Here, we used primary human fibroblasts made senescent by replicative exhaustion, doxorubicin or hydrogen peroxide treatment, and examined the number of mitochondria and the levels of mitochondrial respiration, mitochondrial DNA methylation and the mitochondria-encoded peptides humanin, MOTS-c, SHLP2 and SHLP6.
  5. 05LabIn vitro (cells)Efficacy outcome

    In doxorubicin-induced senescent human fibroblasts, humanin and MOTS-c administration modestly increased selected components of the SASP.

    In plain wordsIn lab tests on senescent human cells, humanin and MOTS-c modestly increased some senescence-associated secretory components.

    Peptide
    Humanin
    Outcome
    IncreaseSASP components after humanin and MOTS-c
    Study

    humann: not reported in source

    primary human fibroblasts made senescent
    Outcome group
    Inflammation markers · Aging and longevity
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Humanin and MOTS-c administration modestly increased mitochondrial respiration and selected components of the SASP in doxorubicin-induced senescent cells partially via JAK pathway.
    1 context sentence
    Summary · context
    Here, we used primary human fibroblasts made senescent by replicative exhaustion, doxorubicin or hydrogen peroxide treatment, and examined the number of mitochondria and the levels of mitochondrial respiration, mitochondrial DNA methylation and the mitochondria-encoded peptides humanin, MOTS-c, SHLP2 and SHLP6.
  6. 06LabIn vitro (cells)Mechanism

    In doxorubicin-induced senescent human fibroblasts, the effects of humanin and MOTS-c occurred partially via the JAK pathway.

    In plain wordsIn lab tests on senescent human cells, the effects of humanin and MOTS-c worked partly through the JAK pathway.

    Peptide
    Humanin
    Outcome
    Not applicableJAK pathway involvement
    Study

    humann: not reported in source

    primary human fibroblasts made senescent
    Outcome group
    Receptor activity and mechanism · Aging and longevity
    Studied dose
    Dose not stated

    Source sentences

    Summary
    partially via JAK pathway.
    1 context sentence
    Summary · context
    Here, we used primary human fibroblasts made senescent by replicative exhaustion, doxorubicin or hydrogen peroxide treatment, and examined the number of mitochondria and the levels of mitochondrial respiration, mitochondrial DNA methylation and the mitochondria-encoded peptides humanin, MOTS-c, SHLP2 and SHLP6.

Natural levels measured2

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.

  1. 07LabEndogenous levelIn vitro (cells)Other

    In primary human fibroblasts, senescent cells had elevated levels of MOTS‑c.

    In plain wordsIn lab-grown human cells, aged (senescent) cells carried more of the cells' own MOTS‑c.

    Peptide
    MOTS-c
    Outcome
    IncreaseMOTS-c level in senescent cells
    Study

    humann: not reported in source

    primary human fibroblasts made senescent
    Outcome group
    Endogenous peptide levels · Aging and longevity

    Source sentences

    Summary
    elevated levels of humanin and MOTS-c.
    1 context sentence
    Summary · context
    Here, we used primary human fibroblasts made senescent by replicative exhaustion, doxorubicin or hydrogen peroxide treatment, and examined the number of mitochondria and the levels of mitochondrial respiration, mitochondrial DNA methylation and the mitochondria-encoded peptides humanin, MOTS-c, SHLP2 and SHLP6.

    This result measures the body's own MOTS-c. Nobody was given the peptide. It is not evidence about taking it.

  2. 08LabEndogenous levelIn vitro (cells)Other

    In primary human fibroblasts made senescent, the cells' own humanin levels were elevated, together with MOTS-c.

    In plain wordsIn senescent human cells in the lab, the body's own humanin levels were higher.

    Peptide
    Humanin
    Outcome
    IncreaseHumanin level in senescent cells
    Study

    humann: not reported in source

    primary human fibroblasts made senescent
    Outcome group
    Aging markers · Aging and longevity

    Source sentences

    Summary
    Senescent cells showed increased numbers of mitochondria and higher levels of mitochondrial respiration, variable changes in mitochondrial DNA methylation, and elevated levels of humanin and MOTS-c.
    1 context sentence
    Summary · context
    Here, we used primary human fibroblasts made senescent by replicative exhaustion, doxorubicin or hydrogen peroxide treatment, and examined the number of mitochondria and the levels of mitochondrial respiration, mitochondrial DNA methylation and the mitochondria-encoded peptides humanin, MOTS-c, SHLP2 and SHLP6.

    This result measures the body's own Humanin. Nobody was given the peptide. It is not evidence about taking it.

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. Versions 4 to 18Current

    28 Oct 2026, 02:02 UTC

    The same notice was added 15 times, first on 13 Oct 2026, 21:44 UTC. The status did not change between them.

    Study results updated

  2. Version 3

    13 Oct 2026, 16:31 UTC

    Study data updated · source update from Europe PMC

  3. Version 2

    10 Oct 2026, 08:19 UTC

    Study results updated

  4. 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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