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Study · Other design · mouse · 2020

3 results

AMPK Activation by 5-Amino-4-Imidazole Carboxamide Riboside-1-β-D-Ribofuranoside Attenuates Alkali Injury-Induced Corneal Fibrosis.

Nuwormegbe SA, Kim SW

Investigative ophthalmology & visual science1 Jun 2020Cited by 11 (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: CC BY-NC-ND. Results still quote short attributed sentences.

Results from this study3

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

  1. 01AnimalOther designMechanism

    In corneal injury models, AICAR-mediated AMPK activation significantly suppressed TGF-β1 expression.

    In plain wordsIn mice and lab tests with human corneal cells, AICAR significantly decreased TGF-β1 expression.

    Outcome
    DecreaseTGF-β1 expression
    Study

    mouse and humann: not reported in source

    corneal alkali injury and TGF-β1-treated corneal fibroblasts
    Outcome group
    Receptor activity and mechanism · Eye
    Studied dose
    Dose not stated

    Source sentences

    Summary
    AMPK activation by AICAR significantly suppressed TGF-β1 and ECM protein expression.
    2 context sentences
    Summary · context
    Mouse models of corneal alkali burn, produced by placing 2-mm-diameter filter paper soaked in 0.1-N NaOH on the right cornea for 30 seconds, were treated with the test drugs 4× daily for 21 days.
    Summary · context
    For in vitro analysis, primary human corneal fibroblasts were treated directly with TGF-β1 to induce fibrosis, with or without AICAR pretreatment.
  2. 02AnimalOther designMechanism

    In corneal injury models, AICAR-mediated AMPK activation significantly suppressed ECM protein expression.

    In plain wordsIn mice and lab tests with human corneal cells, AICAR significantly decreased extracellular matrix protein expression.

    Outcome
    DecreaseECM protein expression
    Study

    mouse and humann: not reported in source

    corneal alkali injury and TGF-β1-treated corneal fibroblasts
    Outcome group
    Receptor activity and mechanism · Eye
    Studied dose
    Dose not stated

    Source sentences

    Summary
    AMPK activation by AICAR significantly suppressed TGF-β1 and ECM protein expression.
    2 context sentences
    Summary · context
    Mouse models of corneal alkali burn, produced by placing 2-mm-diameter filter paper soaked in 0.1-N NaOH on the right cornea for 30 seconds, were treated with the test drugs 4× daily for 21 days.
    Summary · context
    For in vitro analysis, primary human corneal fibroblasts were treated directly with TGF-β1 to induce fibrosis, with or without AICAR pretreatment.

Studies that did not test the peptide alone1

In this study, AICAR (acadesine) 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 AICAR (acadesine).

  1. 03AnimalNot a test of AICAR (acadesine) aloneOther designMechanism

    In corneal injury models, Compound C attenuated the antifibrotic response to AICAR, supporting AMPK dependence.

    In plain wordsIn mice and lab tests with human corneal cells, Compound C reduced the antifibrotic response to AICAR.

    Outcome
    DecreaseAMPK dependence of antifibrotic response
    Study

    mouse and humann: not reported in source

    corneal alkali injury and TGF-β1-treated corneal fibroblasts
    Outcome group
    Receptor activity and mechanism · Eye

    Source sentences

    Summary
    The antifibrotic effect of AICAR was AMPK dependent, as treatment with the AMPK inhibitor Compound C attenuated the antifibrotic response.
    2 context sentences
    Summary · context
    Mouse models of corneal alkali burn, produced by placing 2-mm-diameter filter paper soaked in 0.1-N NaOH on the right cornea for 30 seconds, were treated with the test drugs 4× daily for 21 days.
    Summary · context
    For in vitro analysis, primary human corneal fibroblasts were treated directly with TGF-β1 to induce fibrosis, with or without AICAR pretreatment.

    In this study, AICAR (acadesine) 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 AICAR (acadesine).

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

    21 Oct 2026, 15:58 UTC

    Study results updated

  2. Version 1

    21 Oct 2026, 12:50 UTC

    First added · source update from Europe PMC

Subjects

Terms as the source lists them.

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