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Study · In vitro (cells) · 2016

12 results

The Mitochondrial-Derived Peptide Humanin Protects RPE Cells From Oxidative Stress, Senescence, and Mitochondrial Dysfunction.

Sreekumar PG, Ishikawa K, Spee C, Mehta HH, Wan J, Yen K, Cohen P, Kannan R, Hinton DR

Investigative ophthalmology & visual science1 Mar 2016Cited by 160 (Europe PMC)

Summary

The text of this summary is not shown here, because the article license does not allow reuse. Read it at the source (opens in a new tab)

Text rights: CC BY-NC-ND. Results still quote short attributed sentences.

Results from this study12

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

  1. 01LabIn vitro (cells)Efficacy outcome

    In human RPE cells, humanin cotreatment inhibited tBH-induced reactive oxygen species formation.

    In plain wordsIn lab tests on human eye cells, humanin reduced the formation of reactive oxygen species caused by an oxidant.

    Peptide
    Humanin
    Outcome
    DecreaseOxidant-induced reactive oxygen species formation
    Study

    humann: not reported in source

    Human retinal pigment epithelial (hRPE) cells
    Comparator
    tBH without humanin
    Outcome group
    Mitochondrial function · Eye
    Studied dose
    0.5-10 μg/mL · 24 hoursAs given in this study (human).

    Source sentences

    Summary
    Humanin cotreatment inhibited tBH-induced reactive oxygen species formation
    1 context sentence
    Summary · context
    Human RPE cells were treated with 150 μM tert-Butyl hydroperoxide (tBH) in the absence/presence of HN (0.5-10 μg/mL) for 24 hours.
  2. 02LabIn vitro (cells)Efficacy outcome

    In human RPE cells, humanin cotreatment restored mitochondrial bioenergetics and prevented the decrease caused by oxidative stress.

    In plain wordsIn lab tests on human eye cells, humanin kept mitochondrial energy production from falling under oxidative stress.

    Peptide
    Humanin
    Outcome
    IncreaseMitochondrial bioenergetics under oxidative stress
    Study

    humann: not reported in source

    Human retinal pigment epithelial (hRPE) cells
    Comparator
    tBH without humanin
    Outcome group
    Mitochondrial function · Eye
    Studied dose
    0.5-10 μg/mL · 24 hoursAs given in this study (human).

    Source sentences

    Summary
    significantly restored mitochondrial bioenergetics in hRPE cells.
    2 context sentences
    Summary · context
    The oxidative stress-induced decrease in mitochondrial bioenergetics was prevented by HN cotreatment.
    Summary · context
    Human RPE cells were treated with 150 μM tert-Butyl hydroperoxide (tBH) in the absence/presence of HN (0.5-10 μg/mL) for 24 hours.
  3. 03LabIn vitro (cells)Mechanism

    In human RPE cells, exogenous humanin was taken up by the cells and colocalized with mitochondria.

    In plain wordsIn lab tests on human eye cells, added humanin entered the cells and was found alongside mitochondria.

    Peptide
    Humanin
    Outcome
    Not applicableExogenous humanin uptake and mitochondrial colocalization
    Study

    humann: not reported in source

    Human retinal pigment epithelial (hRPE) cells
    Comparator
    tBH without humanin
    Outcome group
    Mitochondrial function · Eye
    Studied dose
    0.5-10 μg/mL · 24 hoursAs given in this study (human).

    Source sentences

    Summary
    Exogenous HN was taken up by RPE and colocalized with mitochondria.
    1 context sentence
    Summary · context
    Human RPE cells were treated with 150 μM tert-Butyl hydroperoxide (tBH) in the absence/presence of HN (0.5-10 μg/mL) for 24 hours.
  4. 04LabIn vitro (cells)Mechanism

    In human RPE cells, humanin treatment increased mitochondrial DNA copy number.

    In plain wordsIn lab tests on human eye cells, humanin raised the number of mitochondrial DNA copies.

    Peptide
    Humanin
    Outcome
    IncreaseMitochondrial DNA copy number
    Study

    humann: not reported in source

    Human retinal pigment epithelial (hRPE) cells
    Comparator
    tBH without humanin
    Outcome group
    Mitochondrial function · Eye
    Studied dose
    0.5-10 μg/mL · 24 hoursAs given in this study (human).

    Source sentences

    Summary
    Humanin treatment increased mitochondrial DNA copy number
    1 context sentence
    Summary · context
    Human RPE cells were treated with 150 μM tert-Butyl hydroperoxide (tBH) in the absence/presence of HN (0.5-10 μg/mL) for 24 hours.
  5. 05LabIn vitro (cells)Mechanism

    In human RPE cells, humanin treatment upregulated mitochondrial transcription factor A, a key biogenesis regulator protein.

    In plain wordsIn lab tests on human eye cells, humanin raised levels of a protein that controls mitochondria production.

    Peptide
    Humanin
    Outcome
    IncreaseMitochondrial transcription factor A expression
    Study

    humann: not reported in source

    Human retinal pigment epithelial (hRPE) cells
    Comparator
    tBH without humanin
    Outcome group
    Mitochondrial function · Eye
    Studied dose
    0.5-10 μg/mL · 24 hoursAs given in this study (human).

    Source sentences

    Summary
    upregulated mitochondrial transcription factor A, a key biogenesis regulator protein.
    1 context sentence
    Summary · context
    Human RPE cells were treated with 150 μM tert-Butyl hydroperoxide (tBH) in the absence/presence of HN (0.5-10 μg/mL) for 24 hours.
  6. 06LabIn vitro (cells)Efficacy outcome

    In human RPE cells, humanin protected against oxidative stress-induced cell death.

    In plain wordsIn lab tests on human eye cells, humanin protected the cells from death caused by oxidative stress.

    Peptide
    Humanin
    Outcome
    DecreaseOxidative stress-induced RPE cell death
    Study

    humann: not reported in source

    Human retinal pigment epithelial (hRPE) cells
    Comparator
    tBH without humanin
    Outcome group
    Neuroprotection · Eye
    Studied dose
    0.5-10 μg/mL · 24 hoursAs given in this study (human).

    Source sentences

    Summary
    Humanin protected RPE cells from oxidative stress-induced cell death
    1 context sentence
    Summary · context
    Human RPE cells were treated with 150 μM tert-Butyl hydroperoxide (tBH) in the absence/presence of HN (0.5-10 μg/mL) for 24 hours.
  7. 07LabIn vitro (cells)Mechanism

    In human RPE cells under oxidative stress, humanin inhibited caspase-3 activation.

    In plain wordsIn lab tests on human eye cells, humanin blocked activation of caspase-3, a cell death enzyme.

    Peptide
    Humanin
    Outcome
    DecreaseCaspase-3 activation
    Study

    humann: not reported in source

    Human retinal pigment epithelial (hRPE) cells
    Comparator
    tBH without humanin
    Outcome group
    Neuroprotection · Eye
    Studied dose
    0.5-10 μg/mL · 24 hoursAs given in this study (human).

    Source sentences

    Summary
    inhibiting caspase-3 activation.
    1 context sentence
    Summary · context
    Human RPE cells were treated with 150 μM tert-Butyl hydroperoxide (tBH) in the absence/presence of HN (0.5-10 μg/mL) for 24 hours.
  8. 08LabIn vitro (cells)Mechanism

    In human RPE cells under oxidative stress, humanin protection from cell death involved STAT3 phosphorylation.

    In plain wordsIn lab tests on human eye cells, humanin protected cells in a way linked to STAT3 activation.

    Peptide
    Humanin
    Outcome
    IncreaseSTAT3 phosphorylation
    Study

    humann: not reported in source

    Human retinal pigment epithelial (hRPE) cells
    Comparator
    tBH without humanin
    Outcome group
    Neuroprotection · Eye
    Studied dose
    0.5-10 μg/mL · 24 hoursAs given in this study (human).

    Source sentences

    Summary
    by STAT3 phosphorylation
    1 context sentence
    Summary · context
    Human RPE cells were treated with 150 μM tert-Butyl hydroperoxide (tBH) in the absence/presence of HN (0.5-10 μg/mL) for 24 hours.
  9. 09LabIn vitro (cells)Efficacy outcome

    In human RPE cells, humanin treatment inhibited oxidant-induced senescence.

    In plain wordsIn lab tests on human eye cells, humanin reduced cell aging (senescence) caused by an oxidant.

    Peptide
    Humanin
    Outcome
    DecreaseOxidant-induced senescence
    Study

    humann: not reported in source

    Human retinal pigment epithelial (hRPE) cells
    Comparator
    tBH without humanin
    Outcome group
    Aging markers · Aging and longevity
    Studied dose
    0.5-10 μg/mL · 24 hoursAs given in this study (human).

    Source sentences

    Summary
    Humanin treatment inhibited oxidant-induced senescence.
    1 context sentence
    Summary · context
    Human RPE cells were treated with 150 μM tert-Butyl hydroperoxide (tBH) in the absence/presence of HN (0.5-10 μg/mL) for 24 hours.

Natural levels measured3

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. 10LabEndogenous levelIn vitro (cells)Mechanism

    In human RPE cells, natural humanin localized prominently to the cytoplasmic and mitochondrial compartments.

    In plain wordsIn human eye cells grown in the lab, the cells' own humanin was found mainly in the cytoplasm and mitochondria.

    Peptide
    Humanin
    Outcome
    Not applicableHumanin localization in RPE cells
    Study

    humann: not reported in source

    Human retinal pigment epithelial (hRPE) cells
    Outcome group
    Mitochondrial function · Eye

    Source sentences

    Summary
    Humanin localization in RPE cells and polarized RPE monolayers was assessed by confocal microscopy.
    1 context sentence
    Summary · context
    A prominent localization of HN was found in the cytoplasmic and mitochondrial compartments of hRPE.

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

  2. 11LabEndogenous levelIn vitro (cells)Mechanism

    In human RPE cells, polarized RPE showed elevated cellular natural humanin.

    In plain wordsIn lab tests on human eye cells, polarized cells had higher levels of the cells' own humanin.

    Peptide
    Humanin
    Outcome
    IncreaseCellular humanin in polarized RPE
    Study

    humann: not reported in source

    Human retinal pigment epithelial (hRPE) cells
    Comparator
    Non-polarized RPE
    Outcome group
    Mitochondrial function · Eye

    Source sentences

    Summary
    Polarized RPE demonstrated elevated cellular HN and increased resistance to cell death.

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

  3. 12LabEndogenous levelIn vitro (cells)Mechanism

    In human RPE cells, polarized RPE showed increased resistance to cell death, together with elevated natural humanin.

    In plain wordsIn lab tests on human eye cells, polarized cells with more of their own humanin resisted cell death better.

    Peptide
    Humanin
    Outcome
    IncreaseResistance to cell death in polarized RPE
    Study

    humann: not reported in source

    Human retinal pigment epithelial (hRPE) cells
    Comparator
    Non-polarized RPE
    Outcome group
    Neuroprotection · Eye

    Source sentences

    Summary
    increased resistance to cell death.

    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. Version 2Current

    13 Oct 2026, 21:44 UTC

    Study results updated

  2. Version 1

    13 Oct 2026, 16:31 UTC

    First added · source update from Europe PMC

Subjects

Terms as the source lists them.

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