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Study · Animal study (in vivo) · mouse · 2026

1 result

Peroxiredoxin Ⅲ safeguards cardiac function against doxorubicin by regulating mitochondrial quality control via H2O2 detoxification.

Park JW, Jang SY, Kim MY, Yi HJ, Sonn SK, Kweon O, Lee BH, Oh GT, Woo HA, Chang TS

Redox biology16 Apr 2026

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 study1

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

  1. 01AnimalAnimal study (in vivo)Efficacy outcome

    In PrxIII knockout mice with doxorubicin cardiotoxicity, SS‑31 rescued the exacerbated cardiac dysfunction.

    In plain wordsIn mice lacking PrxIII and given doxorubicin, SS‑31 rescued the worsened heart function.

    Outcome
    DecreaseDoxorubicin-induced cardiac dysfunction
    Study

    mousen: not reported in source

    PrxIII knockout mice with doxorubicin cardiotoxicity
    Outcome group
    Heart function · Cardiovascular
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Notably, mitigating the mitochondrial H2O2 burden and protecting the mitochondrial inner membrane using the mitochondria-targeted antioxidant peptide SS-31 successfully rescued this exacerbated cardiac dysfunction.
    1 context sentence
    Summary · context
    In vivo experiments using PrxⅢ knockout mice confirmed that loss of PrxⅢ aggravated DOX-induced cardiac dysfunction.

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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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