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Study · In vitro (cells) · 2018

2 results

Cardiomyocyte hypertrophy induced by Endonuclease G deficiency requires reactive oxygen radicals accumulation and is inhibitable by the micropeptide humanin.

Blasco N, Cámara Y, Núñez E, Beà A, Barés G, Forné C, Ruíz-Meana M, Girón C, Barba I, García-Arumí E, García-Dorado D, Vázquez J, Martí R, Llovera M, Sanchis D

Redox biology1 Mar 2018Cited by 40 (Europe PMC)

PMID29502044 (opens in a new tab)PMCIDPMC5952880 (opens in a new tab)DOI10.1016/j.redox.2018.02.021 (opens in a new tab)PepBankPUB-29502044
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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 study2

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

  1. 01LabIn vitro (cells)Mechanism

    In Endog-deficient cardiomyocytes, nanomolar synthetic humanin restored normal ROS levels.

    In plain wordsIn heart cells lacking ENDOG, humanin brought reactive oxygen levels back to normal.

    Peptide
    Humanin
    Outcome
    DecreaseROS levels in Endog-deficient cardiomyocytes
    Study

    n: not reported in source

    Endog-deficient neonatal rodent cardiomyocytes
    Comparator
    Endog-deficient cells without humanin
    Outcome group
    Mitochondrial function · Cardiovascular
    Studied dose
    nanomolar concentrationsAs given in this study.

    Source sentences

    Summary
    Nanomolar concentrations of synthetic humanin restored normal ROS levels
    1 context sentence
    Summary · context
    Endog deficiency induced reactive oxygen species (ROS) accumulation and abnormal growth in neonatal rodent cardiomyocytes, altering the AKT-GSK3β and Class-II histone deacethylases (HDAC) signal transduction pathways.
  2. 02LabIn vitro (cells)Efficacy outcome

    In Endog-deficient cardiomyocytes, nanomolar synthetic humanin restored normal cell size.

    In plain wordsIn heart cells lacking ENDOG, humanin brought cell size back to normal.

    Peptide
    Humanin
    Outcome
    DecreaseCell size in Endog-deficient cardiomyocytes
    Study

    n: not reported in source

    Endog-deficient neonatal rodent cardiomyocytes
    Comparator
    Endog-deficient cells without humanin
    Outcome group
    Heart function · Cardiovascular
    Studied dose
    nanomolar concentrationsAs given in this study.

    Source sentences

    Summary
    Nanomolar concentrations of synthetic humanin restored normal ROS levels and cell size in Endog-deficient cardiomyocytes.
    1 context sentence
    Summary · context
    Endog deficiency induced reactive oxygen species (ROS) accumulation and abnormal growth in neonatal rodent cardiomyocytes, altering the AKT-GSK3β and Class-II histone deacethylases (HDAC) signal transduction pathways.

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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