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Study · Not a test of the peptide alone · 2014

3 results

Reactive oxygen species regulation of autophagy in skeletal muscles.

Rahman M, Mofarrahi M, Kristof AS, Nkengfac B, Harel S, Hussain SN

Antioxidants & redox signaling1 Jan 2014Cited by 82 (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 study3

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

Studies that did not test the peptide alone3

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. 01LabNot a test of Elamipretide (SS-31) aloneIn vitro (cells)Mechanism

    In C2C12 myotubes, preincubation with antioxidants including SS31 (pooled with tempol, NAC and mito-tempol) significantly decreased long-lived protein degradation.

    In plain wordsIn lab-grown muscle cells, a group of antioxidants that included SS31 slowed protein breakdown; SS31 alone was not reported.

    Outcome
    DecreaseLong-lived protein degradation
    Study

    n: not reported in source

    Differentiated C2C12 myotubes
    Outcome group
    Muscle injury and repair · Musculoskeletal

    Source sentences

    Summary
    Preincubation with the general antioxidants tempol (superoxide dismutase mimic) and N-acetyl cysteine (NAC) or the mitochondria-specific antioxidants mito-tempol and SS31 significantly decreased the rates of long-lived protein degradation and LC3B flux and blocked the induction of autophagy-related gene expression.
    2 context sentences
    Summary · context
    To evaluate the effects of physiological levels of mitochondrial-derived reactive oxygen species (ROS) on skeletal muscle autophagy, a proteolytic pathway designed to regulate contractile and myofilament homeostasis and to recycle long-lived proteins and damaged organelles.
    Summary · context
    Basal levels of autophagy and autophagy triggered by 1.5 to 4 h of acute nutrient deprivation, rapamycin treatment, or leucine deprivation were measured in differentiated C2C12 myotubes using long-lived protein degradation assays, LC3B lipidation, autophagy-related gene expression, and electron microscopy.

    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).

  2. 02LabNot a test of Elamipretide (SS-31) aloneIn vitro (cells)Mechanism

    In C2C12 myotubes, preincubation with antioxidants including SS31 (pooled with tempol, NAC and mito-tempol) significantly decreased LC3B flux.

    In plain wordsIn lab-grown muscle cells, a group of antioxidants that included SS31 lowered a marker of autophagy; SS31 alone was not reported.

    Outcome
    DecreaseLC3B flux
    Study

    n: not reported in source

    Differentiated C2C12 myotubes
    Outcome group
    Muscle injury and repair · Musculoskeletal

    Source sentences

    Summary
    Preincubation with the general antioxidants tempol (superoxide dismutase mimic) and N-acetyl cysteine (NAC) or the mitochondria-specific antioxidants mito-tempol and SS31 significantly decreased the rates of long-lived protein degradation and LC3B flux and blocked the induction of autophagy-related gene expression.
    2 context sentences
    Summary · context
    To evaluate the effects of physiological levels of mitochondrial-derived reactive oxygen species (ROS) on skeletal muscle autophagy, a proteolytic pathway designed to regulate contractile and myofilament homeostasis and to recycle long-lived proteins and damaged organelles.
    Summary · context
    Basal levels of autophagy and autophagy triggered by 1.5 to 4 h of acute nutrient deprivation, rapamycin treatment, or leucine deprivation were measured in differentiated C2C12 myotubes using long-lived protein degradation assays, LC3B lipidation, autophagy-related gene expression, and electron microscopy.

    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).

  3. 03LabNot a test of Elamipretide (SS-31) aloneIn vitro (cells)Mechanism

    In C2C12 myotubes, preincubation with antioxidants including SS31 (pooled with tempol, NAC and mito-tempol) blocked the induction of autophagy-related gene expression.

    In plain wordsIn lab-grown muscle cells, a group of antioxidants that included SS31 blocked autophagy gene activation; SS31 alone was not reported.

    Outcome
    DecreaseAutophagy-related gene expression
    Study

    n: not reported in source

    Differentiated C2C12 myotubes
    Outcome group
    Muscle injury and repair · Musculoskeletal

    Source sentences

    Summary
    Preincubation with the general antioxidants tempol (superoxide dismutase mimic) and N-acetyl cysteine (NAC) or the mitochondria-specific antioxidants mito-tempol and SS31 significantly decreased the rates of long-lived protein degradation and LC3B flux and blocked the induction of autophagy-related gene expression.
    2 context sentences
    Summary · context
    To evaluate the effects of physiological levels of mitochondrial-derived reactive oxygen species (ROS) on skeletal muscle autophagy, a proteolytic pathway designed to regulate contractile and myofilament homeostasis and to recycle long-lived proteins and damaged organelles.
    Summary · context
    Basal levels of autophagy and autophagy triggered by 1.5 to 4 h of acute nutrient deprivation, rapamycin treatment, or leucine deprivation were measured in differentiated C2C12 myotubes using long-lived protein degradation assays, LC3B lipidation, autophagy-related gene expression, and electron microscopy.

    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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