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

7 results

Orforglipron alleviates aortic aneurysm and dissection via inhibiting WNT5A noncanonical signaling.

Deng Y, Guo Z, Yu L, Zhang J, Qian J, Wang J, Chen X, Xu Z, Wang D, Kong C

Biochemical pharmacology27 Jul 2026

PMID42508653 (opens in a new tab)DOI10.1016/j.bcp.2026.118294 (opens in a new tab)PepBankPUB-42508653
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 study7

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

  1. 01AnimalAnimal study (in vivo)Efficacy outcome

    In humanized GLP-1R mice with induced AAD, orforglipron protected against smooth muscle cell phenotypic switching.

    In plain wordsIn mice with induced aortic disease, orforglipron reduced smooth muscle cell phenotypic switching.

    Peptide
    Orforglipron
    Outcome
    DecreaseSmooth muscle cell phenotypic switching
    Study

    mousen: not reported in source

    Male B6 humanized GLP-1R mice with induced AAD
    Outcome group
    Receptor activity and mechanism · Cardiovascular
    Studied dose
    Dose not stated · oral gavage · 28 consecutive daysAs given in this study (mouse).

    Source sentences

    Summary
    Orforglipron treatment protected mice from smooth muscle cell phenotypic switching, medial degeneration, and AAD formation.
    1 context sentence
    Summary · context
    In this study, male B6 humanized GLP-1R mice were treated with orforglipron by oral gavage for 28 consecutive days and subjected to beta-aminopropionitrile combined with angiotensin II infusion to induce AAD.
  2. 02AnimalAnimal study (in vivo)Efficacy outcome

    In humanized GLP-1R mice with induced AAD, orforglipron protected against medial degeneration.

    In plain wordsIn mice with induced aortic disease, orforglipron protected against degeneration of the artery wall.

    Peptide
    Orforglipron
    Outcome
    DecreaseMedial degeneration
    Study

    mousen: not reported in source

    Male B6 humanized GLP-1R mice with induced AAD
    Outcome group
    Vascular function · Cardiovascular
    Studied dose
    Dose not stated · oral gavage · 28 consecutive daysAs given in this study (mouse).

    Source sentences

    Summary
    Orforglipron treatment protected mice from smooth muscle cell phenotypic switching, medial degeneration, and AAD formation.
    1 context sentence
    Summary · context
    In this study, male B6 humanized GLP-1R mice were treated with orforglipron by oral gavage for 28 consecutive days and subjected to beta-aminopropionitrile combined with angiotensin II infusion to induce AAD.
  3. 03AnimalAnimal study (in vivo)Efficacy outcome

    In humanized GLP-1R mice, orforglipron protected against induced aortic aneurysm and dissection formation.

    In plain wordsIn mice, orforglipron protected against induced aortic aneurysm and dissection.

    Peptide
    Orforglipron
    Outcome
    DecreaseAAD formation
    Study

    mousen: not reported in source

    Male B6 humanized GLP-1R mice with induced AAD
    Outcome group
    Cardiovascular events · Cardiovascular
    Studied dose
    Dose not stated · oral gavage · 28 consecutive daysAs given in this study (mouse).

    Source sentences

    Summary
    Orforglipron treatment protected mice from smooth muscle cell phenotypic switching, medial degeneration, and AAD formation.
    1 context sentence
    Summary · context
    In this study, male B6 humanized GLP-1R mice were treated with orforglipron by oral gavage for 28 consecutive days and subjected to beta-aminopropionitrile combined with angiotensin II infusion to induce AAD.
  4. 04LabIn vitro (cells)Mechanism

    In RNA sequencing analysis of human aortic smooth muscle cells, Wnt5a was identified as a downstream target regulated by orforglipron.

    In plain wordsIn cells, RNA sequencing identified Wnt5a as a target regulated by orforglipron.

    Peptide
    Orforglipron
    Outcome
    Not applicableWnt5a downstream target identification
    Study

    humann: not reported in source

    Human aortic smooth muscle cells
    Outcome group
    Receptor activity and mechanism · Cardiovascular
    Studied dose
    Dose not stated

    Source sentences

    Summary
    RNA sequencing of human aortic smooth muscle cells identified Wnt5a as a key downstream target regulated by orforglipron.
  5. 05LabOther designMechanism

    In mechanistic experiments, orforglipron inhibited ERK phosphorylation.

    In plain wordsIn lab tests, orforglipron reduced ERK phosphorylation.

    Peptide
    Orforglipron
    Outcome
    DecreaseERK phosphorylation
    Study

    n: not reported in source

    Outcome group
    Receptor activity and mechanism · Cardiovascular
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Mechanistically, orforglipron inhibited ERK phosphorylation, reduced EGR1 expression, and thereby suppressed EGR1-mediated Wnt5a transcription.
  6. 06LabOther designMechanism

    In mechanistic experiments, orforglipron reduced EGR1 expression.

    In plain wordsIn lab tests, orforglipron reduced EGR1 expression.

    Peptide
    Orforglipron
    Outcome
    DecreaseEGR1 expression
    Study

    n: not reported in source

    Outcome group
    Receptor activity and mechanism · Cardiovascular
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Mechanistically, orforglipron inhibited ERK phosphorylation, reduced EGR1 expression, and thereby suppressed EGR1-mediated Wnt5a transcription.
  7. 07LabOther designMechanism

    In mechanistic experiments, orforglipron suppressed EGR1-mediated Wnt5a transcription.

    In plain wordsIn lab tests, orforglipron reduced EGR1-mediated Wnt5a transcription.

    Peptide
    Orforglipron
    Outcome
    DecreaseEGR1-mediated Wnt5a transcription
    Study

    n: not reported in source

    Outcome group
    Receptor activity and mechanism · Cardiovascular
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Mechanistically, orforglipron inhibited ERK phosphorylation, reduced EGR1 expression, and thereby suppressed EGR1-mediated Wnt5a transcription.

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

    14 Oct 2026, 05:02 UTC

    Study results updated

  2. Version 1

    14 Oct 2026, 01:46 UTC

    First added · source update from Europe PMC

Subjects

Terms as the source lists them.

Publication types

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