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Study · In vitro (cells) · 2018

8 results

Elamipretide Promotes Mitophagosome Formation and Prevents Its Reduction Induced by Nutrient Excess in INS1 β-cells.

Petcherski A, Trudeau KM, Wolf DM, Segawa M, Lee J, Taddeo EP, Deeney JT, Liesa M

Journal of molecular biology30 Oct 2018Cited by 16 (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: Publisher copyright. Results still quote short attributed sentences.

Results from this study8

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

  1. 01LabIn vitro (cells)Mechanism

    In control INS1 β-cells, elamipretide increased the engulfment of mitochondria into autophagosomes.

    In plain wordsIn cells, elamipretide increased the uptake of mitochondria into autophagosomes in normal insulin-producing cells.

    Outcome
    IncreaseEngulfment of mitochondria into autophagosomes in control cells
    Study

    n: not reported in source

    INS1 β-cells
    Outcome group
    Mitochondrial function · Metabolic and weight
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Elamipretide treatment was sufficient to increase engulfment of mitochondria into autophagosomes in control INS1 β-cells, without inducing widespread changes in mitochondrial morphology or membrane potential.
    1 context sentence
    Summary · context
    Thus, we tested the effects of elamipretide on mitochondrial morphology, mitophagosome formation, and their early disruption induced by excess nutrients in INS1 β-cells.
  2. 02LabIn vitro (cells)Mechanism

    In control INS1 β-cells, elamipretide did not induce widespread changes in mitochondrial morphology.

    In plain wordsIn cells, elamipretide did not change the shape of mitochondria in normal insulin-producing cells.

    Outcome
    No significant changeMitochondrial morphology in control cells
    Study

    n: not reported in source

    INS1 β-cells
    Outcome group
    Mitochondrial function · Metabolic and weight
    Studied dose
    Dose not stated

    Source sentences

    Summary
    without inducing widespread changes in mitochondrial morphology or membrane potential.
    1 context sentence
    Summary · context
    Thus, we tested the effects of elamipretide on mitochondrial morphology, mitophagosome formation, and their early disruption induced by excess nutrients in INS1 β-cells.
  3. 03LabIn vitro (cells)Mechanism

    In control INS1 β-cells, elamipretide did not induce widespread changes in mitochondrial membrane potential.

    In plain wordsIn cells, elamipretide did not change mitochondrial membrane potential in normal insulin-producing cells.

    Outcome
    No significant changeMitochondrial membrane potential in control cells
    Study

    n: not reported in source

    INS1 β-cells
    Outcome group
    Mitochondrial function · Metabolic and weight
    Studied dose
    Dose not stated

    Source sentences

    Summary
    without inducing widespread changes in mitochondrial morphology or membrane potential.
    1 context sentence
    Summary · context
    Thus, we tested the effects of elamipretide on mitochondrial morphology, mitophagosome formation, and their early disruption induced by excess nutrients in INS1 β-cells.
  4. 04LabIn vitro (cells)Mechanism

    In INS1 β-cells exposed to nutrient excess, elamipretide prevented mitochondrial fragmentation.

    In plain wordsIn cells under nutrient excess, elamipretide prevented mitochondria from breaking into fragments.

    Outcome
    DecreaseMitochondrial fragmentation under nutrient excess
    Study

    n: not reported in source

    INS1 β-cells
    Outcome group
    Mitochondrial function · Metabolic and weight
    Studied dose
    Dose not stated

    Source sentences

    Summary
    In an early pathogenic context mimicked by short-term exposure to nutrient excess, elamipretide treatment prevented both mitochondrial fragmentation and defects in the engulfment of mitochondria into autophagosomes.
    1 context sentence
    Summary · context
    Thus, we tested the effects of elamipretide on mitochondrial morphology, mitophagosome formation, and their early disruption induced by excess nutrients in INS1 β-cells.
  5. 05LabIn vitro (cells)Mechanism

    In INS1 β-cells exposed to nutrient excess, elamipretide prevented the defects in the engulfment of mitochondria into autophagosomes.

    In plain wordsIn cells under nutrient excess, elamipretide prevented the loss of mitochondria uptake into autophagosomes.

    Outcome
    IncreaseEngulfment of mitochondria into autophagosomes under nutrient excess
    Study

    n: not reported in source

    INS1 β-cells
    Outcome group
    Mitochondrial function · Metabolic and weight
    Studied dose
    Dose not stated

    Source sentences

    Summary
    In an early pathogenic context mimicked by short-term exposure to nutrient excess, elamipretide treatment prevented both mitochondrial fragmentation and defects in the engulfment of mitochondria into autophagosomes.
    1 context sentence
    Summary · context
    Thus, we tested the effects of elamipretide on mitochondrial morphology, mitophagosome formation, and their early disruption induced by excess nutrients in INS1 β-cells.
  6. 06LabIn vitro (cells)Mechanism

    In INS1 β-cells exposed to nutrient excess, elamipretide did not prevent lysosomal defects.

    In plain wordsIn cells under nutrient excess, elamipretide did not prevent defects in lysosomes.

    Outcome
    No significant changeLysosomal defects under nutrient excess
    Study

    n: not reported in source

    INS1 β-cells
    Outcome group
    Mitochondrial function · Metabolic and weight
    Studied dose
    Dose not stated

    Source sentences

    Summary
    On the other hand, elamipretide did not prevent lysosomal defects induced by nutrient excess.
    1 context sentence
    Summary · context
    Thus, we tested the effects of elamipretide on mitochondrial morphology, mitophagosome formation, and their early disruption induced by excess nutrients in INS1 β-cells.
  7. 07LabIn vitro (cells)Mechanism

    In INS1 β-cells exposed to nutrient excess, elamipretide did not reduce the pathogenic accumulation of p62 and LC3II.

    In plain wordsIn cells under nutrient excess, elamipretide did not reduce the build-up of p62 and LC3II.

    Outcome
    No significant changep62 and LC3II accumulation under nutrient excess
    Study

    n: not reported in source

    INS1 β-cells
    Outcome group
    Mitochondrial function · Metabolic and weight
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Accordingly, elamipretide treatment did not entail benefits on pathogenic p62 and LC3II accumulation or on insulin secretory function.
    1 context sentence
    Summary · context
    Thus, we tested the effects of elamipretide on mitochondrial morphology, mitophagosome formation, and their early disruption induced by excess nutrients in INS1 β-cells.
  8. 08LabIn vitro (cells)Mechanism

    In INS1 β-cells exposed to nutrient excess, elamipretide did not benefit insulin secretory function.

    In plain wordsIn cells under nutrient excess, elamipretide did not improve insulin release.

    Outcome
    No significant changeInsulin secretory function under nutrient excess
    Study

    n: not reported in source

    INS1 β-cells
    Outcome group
    Glycemic control · Metabolic and weight
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Accordingly, elamipretide treatment did not entail benefits on pathogenic p62 and LC3II accumulation or on insulin secretory function.
    1 context sentence
    Summary · context
    Thus, we tested the effects of elamipretide on mitochondrial morphology, mitophagosome formation, and their early disruption induced by excess nutrients in INS1 β-cells.

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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