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Study · Animal study (in vivo) · mouse · 2017

6 results

Aicar treatment reduces interstitial fibrosis in aging mice: Suppression of the inflammatory fibroblast.

Cieslik KA, Trial J, Entman ML

Journal of molecular and cellular cardiology4 Aug 2017Cited by 26 (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: Publisher copyright. Results still quote short attributed sentences.

Results from this study6

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

  1. 01AnimalAnimal study (in vivo)Mechanism

    In aging mice, AICAR suppressed excessive MCP-1 generation.

    In plain wordsIn mice, AICAR reduced excessive MCP-1 production in aging hearts.

    Outcome
    DecreaseMCP-1 generation
    Study

    mousen: not reported in source

    aging C57BL/6J mice
    Outcome group
    Inflammation markers · Cardiovascular
    Studied dose
    Dose not stated · 30 daysAs given in this study (mouse).

    Source sentences

    Summary
    This treatment suppressed excessive monocyte chemoattractant protein-1 (MCP-1) generation, which diminished leukocyte infiltration and in consequence suppressed the formation of macrophage-derived myeloid fibroblasts.
    1 context sentence
    Summary · context
    Aging C57BL/6J mice were treated with AICAR (an AMPK activator) for a 30-day period.
  2. 02AnimalAnimal study (in vivo)Mechanism

    In aging mice, AICAR treatment diminished leukocyte infiltration.

    In plain wordsIn mice, AICAR reduced white blood cell infiltration in aging hearts.

    Outcome
    DecreaseLeukocyte infiltration
    Study

    mousen: not reported in source

    aging C57BL/6J mice
    Outcome group
    Immune response · Cardiovascular
    Studied dose
    Dose not stated · 30 daysAs given in this study (mouse).

    Source sentences

    Summary
    This treatment suppressed excessive monocyte chemoattractant protein-1 (MCP-1) generation, which diminished leukocyte infiltration and in consequence suppressed the formation of macrophage-derived myeloid fibroblasts.
    1 context sentence
    Summary · context
    Aging C57BL/6J mice were treated with AICAR (an AMPK activator) for a 30-day period.
  3. 03AnimalAnimal study (in vivo)Mechanism

    In aging mice, AICAR suppressed formation of macrophage-derived myeloid fibroblasts.

    In plain wordsIn mice, AICAR reduced formation of myeloid fibroblasts from macrophages in aging hearts.

    Outcome
    DecreaseMyeloid fibroblast formation
    Study

    mousen: not reported in source

    aging C57BL/6J mice
    Outcome group
    Heart function · Cardiovascular
    Studied dose
    Dose not stated · 30 daysAs given in this study (mouse).

    Source sentences

    Summary
    This treatment suppressed excessive monocyte chemoattractant protein-1 (MCP-1) generation, which diminished leukocyte infiltration and in consequence suppressed the formation of macrophage-derived myeloid fibroblasts.
    1 context sentence
    Summary · context
    Aging C57BL/6J mice were treated with AICAR (an AMPK activator) for a 30-day period.
  4. 04AnimalAnimal study (in vivo)Mechanism

    In aging mice, AICAR reduced mesenchymal fibroblast numbers.

    In plain wordsIn mice, AICAR reduced mesenchymal fibroblast numbers in aging hearts.

    Outcome
    DecreaseMesenchymal fibroblast number
    Study

    mousen: not reported in source

    aging C57BL/6J mice
    Outcome group
    Heart function · Cardiovascular
    Studied dose
    Dose not stated · 30 daysAs given in this study (mouse).

    Source sentences

    Summary
    Interestingly, the number of mesenchymal fibroblasts was also reduced.
    1 context sentence
    Summary · context
    Aging C57BL/6J mice were treated with AICAR (an AMPK activator) for a 30-day period.
  5. 05AnimalAnimal study (in vivo)Mechanism

    In aging mice, AICAR reduced collagen type I expression.

    In plain wordsIn mice, AICAR reduced collagen type I expression in aging hearts.

    Outcome
    DecreaseCollagen type I expression
    Study

    mousen: not reported in source

    aging C57BL/6J mice
    Outcome group
    Heart function · Cardiovascular
    Studied dose
    Dose not stated · 30 daysAs given in this study (mouse).

    Source sentences

    Summary
    In addition, we observed changes in extracellular matrix (ECM) deposition, specifically that collagen type I and the alternatively spliced variant of fibronectin (EDA) expressions were reduced.
    1 context sentence
    Summary · context
    Aging C57BL/6J mice were treated with AICAR (an AMPK activator) for a 30-day period.
  6. 06AnimalAnimal study (in vivo)Mechanism

    In aging mice, AICAR reduced expression of the EDA fibronectin variant.

    In plain wordsIn mice, AICAR reduced expression of the EDA fibronectin variant in aging hearts.

    Outcome
    DecreaseEDA fibronectin expression
    Study

    mousen: not reported in source

    aging C57BL/6J mice
    Outcome group
    Heart function · Cardiovascular
    Studied dose
    Dose not stated · 30 daysAs given in this study (mouse).

    Source sentences

    Summary
    In addition, we observed changes in extracellular matrix (ECM) deposition, specifically that collagen type I and the alternatively spliced variant of fibronectin (EDA) expressions were reduced.
    1 context sentence
    Summary · context
    Aging C57BL/6J mice were treated with AICAR (an AMPK activator) for a 30-day period.

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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