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Study · In vitro (cells) · rat · 2019

8 results

Hexarelin protects cardiac H9C2 cells from angiotensin II-induced hypertrophy via the regulation of autophagy.

Agbo E, Li MX, Wang YQ, Saahene RO, Massaro J, Tian GZ

Die Pharmazie1 Aug 2019Cited by 9 (Europe PMC)

PMID31526442 (opens in a new tab)DOI10.1691/ph.2019.9324 (opens in a new tab)PepBankPUB-31526442
Publisher pagePubMedAsk about this study
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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: 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)Activity measurement

    In H9C2 cardiomyocytes, hexarelin significantly suppressed Ang-II-induced hypertrophy.

    In plain wordsIn heart muscle cells, hexarelin reduced the enlargement caused by angiotensin II.

    Peptide
    Hexarelin
    Outcome
    DecreaseAng-II-induced cardiomyocyte hypertrophy
    Study

    ratn: not reported in source

    H9C2 cardiomyocytes with Ang-II-induced hypertrophy
    Outcome group
    Heart function · Cardiovascular
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Ang-II induced cardiomyocyte hypertrophy, oxidative stress, apoptosis and decreased cell survival, all of which were significantly suppressed by hexarelin treatment which also enhanced autophagy in hypertrophic H9C2 cells.
    1 context sentence
    Summary · context
    H9C2 cardiomyocytes were subjected to hypertrophy by angiotensin-II (Ang-II).
  2. 02LabIn vitro (cells)Activity measurement

    In H9C2 cardiomyocytes, hexarelin significantly suppressed Ang-II-induced oxidative stress.

    In plain wordsIn heart muscle cells, hexarelin reduced oxidative stress caused by angiotensin II.

    Peptide
    Hexarelin
    Outcome
    DecreaseAng-II-induced oxidative stress
    Study

    ratn: not reported in source

    H9C2 cardiomyocytes with Ang-II-induced hypertrophy
    Outcome group
    Heart function · Cardiovascular
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Ang-II induced cardiomyocyte hypertrophy, oxidative stress, apoptosis and decreased cell survival, all of which were significantly suppressed by hexarelin treatment which also enhanced autophagy in hypertrophic H9C2 cells.
    1 context sentence
    Summary · context
    H9C2 cardiomyocytes were subjected to hypertrophy by angiotensin-II (Ang-II).
  3. 03LabIn vitro (cells)Activity measurement

    In H9C2 cardiomyocytes, hexarelin significantly suppressed Ang-II-induced apoptosis.

    In plain wordsIn heart muscle cells, hexarelin reduced cell death caused by angiotensin II.

    Peptide
    Hexarelin
    Outcome
    DecreaseAng-II-induced apoptosis
    Study

    ratn: not reported in source

    H9C2 cardiomyocytes with Ang-II-induced hypertrophy
    Outcome group
    Heart function · Cardiovascular
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Ang-II induced cardiomyocyte hypertrophy, oxidative stress, apoptosis and decreased cell survival, all of which were significantly suppressed by hexarelin treatment which also enhanced autophagy in hypertrophic H9C2 cells.
    1 context sentence
    Summary · context
    H9C2 cardiomyocytes were subjected to hypertrophy by angiotensin-II (Ang-II).
  4. 04LabIn vitro (cells)Activity measurement

    In H9C2 cardiomyocytes, hexarelin significantly suppressed the Ang-II-induced decrease in cell survival.

    In plain wordsIn heart muscle cells, hexarelin kept more cells alive after angiotensin II damage.

    Peptide
    Hexarelin
    Outcome
    IncreaseCell survival after Ang-II
    Study

    ratn: not reported in source

    H9C2 cardiomyocytes with Ang-II-induced hypertrophy
    Outcome group
    Heart function · Cardiovascular
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Ang-II induced cardiomyocyte hypertrophy, oxidative stress, apoptosis and decreased cell survival, all of which were significantly suppressed by hexarelin treatment which also enhanced autophagy in hypertrophic H9C2 cells.
    1 context sentence
    Summary · context
    H9C2 cardiomyocytes were subjected to hypertrophy by angiotensin-II (Ang-II).
  5. 05LabIn vitro (cells)Mechanism

    In hypertrophic H9C2 cells, hexarelin enhanced autophagy.

    In plain wordsIn heart muscle cells, hexarelin increased autophagy, the cell clean-up process.

    Peptide
    Hexarelin
    Outcome
    IncreaseAutophagy in hypertrophic cells
    Study

    ratn: not reported in source

    H9C2 cardiomyocytes with Ang-II-induced hypertrophy
    Outcome group
    Heart function · Cardiovascular
    Studied dose
    Dose not stated

    Source sentences

    Summary
    which also enhanced autophagy in hypertrophic H9C2 cells.
    1 context sentence
    Summary · context
    H9C2 cardiomyocytes were subjected to hypertrophy by angiotensin-II (Ang-II).
  6. 06LabIn vitro (cells)Mechanism

    In H9C2 cells, inhibition of hexarelin-induced autophagy by 3-methyladenine abolished the anti-hypertrophic function of hexarelin.

    In plain wordsIn heart muscle cells, blocking autophagy removed hexarelin's effect against cell enlargement.

    Peptide
    Hexarelin
    Outcome
    No significant changeAnti-hypertrophic effect with autophagy inhibitor 3MA
    Study

    ratn: not reported in source

    H9C2 cardiomyocytes with Ang-II-induced hypertrophy
    Outcome group
    Heart function · Cardiovascular
    Studied dose
    Dose not stated

    Source sentences

    Summary
    inhibition of hexarelin induced autophagy by 3-methyladenine (3MA) abolished the anti-hypertrophic function of hexarelin
    1 context sentence
    Summary · context
    H9C2 cardiomyocytes were subjected to hypertrophy by angiotensin-II (Ang-II).
  7. 07LabIn vitro (cells)Mechanism

    In H9C2 cells, inhibition of autophagy by 3-methyladenine abrogated hexarelin protection against cell survival inhibition and apoptosis.

    In plain wordsIn heart muscle cells, blocking autophagy removed hexarelin's protection of cell survival and against cell death.

    Peptide
    Hexarelin
    Outcome
    No significant changeProtection of survival and apoptosis with autophagy inhibitor 3MA
    Study

    ratn: not reported in source

    H9C2 cardiomyocytes with Ang-II-induced hypertrophy
    Outcome group
    Heart function · Cardiovascular
    Studied dose
    Dose not stated

    Source sentences

    Summary
    also abrogated the protection of hexarelin against cell survival inhibition and apoptosis.
    1 context sentence
    Summary · context
    H9C2 cardiomyocytes were subjected to hypertrophy by angiotensin-II (Ang-II).
  8. 08LabIn vitro (cells)Mechanism

    In H9C2 cells, hexarelin inhibited phosphorylation of mTOR, an upstream regulator of autophagy.

    In plain wordsIn heart muscle cells, hexarelin reduced mTOR activation, a step that controls autophagy.

    Peptide
    Hexarelin
    Outcome
    DecreasemTOR phosphorylation
    Study

    ratn: not reported in source

    H9C2 cardiomyocytes with Ang-II-induced hypertrophy
    Outcome group
    Heart function · Cardiovascular
    Studied dose
    Dose not stated

    Source sentences

    Summary
    hexarelin regulated the upstream signalling of autophagy by inhibiting the phosphorylation of mammalian target of rapamycin(mTOR).
    1 context sentence
    Summary · context
    H9C2 cardiomyocytes were subjected to hypertrophy by angiotensin-II (Ang-II).

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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