Skip to content

Study · Animal study (in vivo) · mouse · 2013

8 results

AICAR-dependent AMPK activation improves scar formation in the aged heart in a murine model of reperfused myocardial infarction.

Cieslik KA, Taffet GE, Crawford JR, Trial J, Mejia Osuna P, Entman ML

Journal of molecular and cellular cardiology19 Jul 2013Cited by 55 (Europe PMC)

PMID23871790 (opens in a new tab)PMCIDPMC3820161 (opens in a new tab)DOI10.1016/j.yjmcc.2013.07.005 (opens in a new tab)PepBankPUB-23871790
Download PDFPubMedAsk about this study
Jump to 8 results

Summary

We have demonstrated that scar formation after myocardial infarction (MI) is associated with an endogenous pool of CD44(pos)CD45(neg) multipotential mesenchymal stem cells (MSC). MSC differentiate into fibroblasts secreting collagen that forms a scar and mature into myofibroblasts that express alpha smooth muscle actin (α-SMA) that stabilizes the scar. In the aging mouse, cardiac repair after MI is associated with impaired differentiation of MSC; MSC derived from the aged hearts form dysfunctional fibroblasts that deposit less collagen in response to transforming growth factor beta-1 (TGF-β1) and poorly mature into myofibroblasts. We found in vitro that the defect in myofibroblast maturation can be remedied by AICAR, which activates non-canonical TGF-β signaling through AMP-activated protein kinase (AMPK). In the present study, we injected aged mice with AICAR and subjected them to 1h occlusion of the left anterior descending artery (LAD) and then reperfusion for up to 30days. AICAR-dependent AMPK signaling led to mobilization of an endogenous CD44(pos)CD45(neg) MSC and its differentiation towards fibroblasts and myofibroblasts in the infarct. This was accompanied by enhanced collagen deposition and collagen fiber maturation in the scar. The AICAR-treated group has demonstrated reduced adverse remodeling as indicated by improved apical end diastolic dimension but no changes in ejection fraction and cardiac output were observed. We concluded that these data indicate the novel, previously not described role of AMPK in the post-MI scar formation. These findings can potentially lead to a new therapeutic strategy for prevention of adverse remodeling in the aging heart.
CC BYText from Europe PMC. Highlighted sentences are the source of results.

Results from this study8

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

  1. 01AnimalAnimal study (in vivo)Efficacy outcome

    In aged mice after myocardial infarction, AICAR-dependent AMPK signaling mobilized endogenous CD44(pos)CD45(neg) mesenchymal stem cells.

    In plain wordsIn mice after a heart attack, AICAR-dependent signaling mobilized the heart's own mesenchymal stem cells.

    Peptide
    AICAR (acadesine)
    Outcome
    IncreaseMSC mobilization
    Study

    mousen: not reported in source

    Aged mice with reperfused myocardial infarction
    Outcome group
    Heart function · Cardiovascular
    Studied dose
    Dose not stated · injectionAs given in this study (mouse).

    Source sentences

    Summary
    AICAR-dependent AMPK signaling led to mobilization of an endogenous CD44(pos)CD45(neg) MSC and its differentiation towards fibroblasts and myofibroblasts in the infarct.
    1 context sentence
    Summary · context
    In the present study, we injected aged mice with AICAR and subjected them to 1h occlusion of the left anterior descending artery (LAD) and then reperfusion for up to 30days.
  2. 02AnimalAnimal study (in vivo)Efficacy outcome

    In aged mice after myocardial infarction, AICAR-dependent AMPK signaling promoted mesenchymal stem cell differentiation toward fibroblasts.

    In plain wordsIn mice after a heart attack, AICAR-dependent signaling promoted stem cell differentiation toward fibroblasts.

    Peptide
    AICAR (acadesine)
    Outcome
    IncreaseFibroblast differentiation
    Study

    mousen: not reported in source

    Aged mice with reperfused myocardial infarction
    Outcome group
    Heart function · Cardiovascular
    Studied dose
    Dose not stated · injectionAs given in this study (mouse).

    Source sentences

    Summary
    AICAR-dependent AMPK signaling led to mobilization of an endogenous CD44(pos)CD45(neg) MSC and its differentiation towards fibroblasts and myofibroblasts in the infarct.
    1 context sentence
    Summary · context
    In the present study, we injected aged mice with AICAR and subjected them to 1h occlusion of the left anterior descending artery (LAD) and then reperfusion for up to 30days.
  3. 03AnimalAnimal study (in vivo)Efficacy outcome

    In aged mice after myocardial infarction, AICAR-dependent AMPK signaling promoted mesenchymal stem cell differentiation toward myofibroblasts.

    In plain wordsIn mice after a heart attack, AICAR-dependent signaling promoted stem cell differentiation toward myofibroblasts.

    Peptide
    AICAR (acadesine)
    Outcome
    IncreaseMyofibroblast differentiation
    Study

    mousen: not reported in source

    Aged mice with reperfused myocardial infarction
    Outcome group
    Heart function · Cardiovascular
    Studied dose
    Dose not stated · injectionAs given in this study (mouse).

    Source sentences

    Summary
    AICAR-dependent AMPK signaling led to mobilization of an endogenous CD44(pos)CD45(neg) MSC and its differentiation towards fibroblasts and myofibroblasts in the infarct.
    1 context sentence
    Summary · context
    In the present study, we injected aged mice with AICAR and subjected them to 1h occlusion of the left anterior descending artery (LAD) and then reperfusion for up to 30days.
  4. 04AnimalAnimal study (in vivo)Efficacy outcome

    In aged mice after myocardial infarction, AICAR treatment enhanced collagen deposition in the scar.

    In plain wordsIn mice after a heart attack, AICAR increased collagen deposition in the scar.

    Peptide
    AICAR (acadesine)
    Outcome
    IncreaseScar collagen deposition
    Study

    mousen: not reported in source

    Aged mice with reperfused myocardial infarction
    Outcome group
    Heart function · Cardiovascular
    Studied dose
    Dose not stated · injectionAs given in this study (mouse).

    Source sentences

    Summary
    This was accompanied by enhanced collagen deposition and collagen fiber maturation in the scar.
    2 context sentences
    Summary · context
    AICAR-dependent AMPK signaling led to mobilization of an endogenous CD44(pos)CD45(neg) MSC and its differentiation towards fibroblasts and myofibroblasts in the infarct.
    Summary · context
    In the present study, we injected aged mice with AICAR and subjected them to 1h occlusion of the left anterior descending artery (LAD) and then reperfusion for up to 30days.
  5. 05AnimalAnimal study (in vivo)Efficacy outcome

    In aged mice after myocardial infarction, AICAR treatment enhanced collagen fiber maturation in the scar.

    In plain wordsIn mice after a heart attack, AICAR improved collagen fiber maturation in the scar.

    Peptide
    AICAR (acadesine)
    Outcome
    IncreaseScar collagen fiber maturation
    Study

    mousen: not reported in source

    Aged mice with reperfused myocardial infarction
    Outcome group
    Heart function · Cardiovascular
    Studied dose
    Dose not stated · injectionAs given in this study (mouse).

    Source sentences

    Summary
    This was accompanied by enhanced collagen deposition and collagen fiber maturation in the scar.
    2 context sentences
    Summary · context
    AICAR-dependent AMPK signaling led to mobilization of an endogenous CD44(pos)CD45(neg) MSC and its differentiation towards fibroblasts and myofibroblasts in the infarct.
    Summary · context
    In the present study, we injected aged mice with AICAR and subjected them to 1h occlusion of the left anterior descending artery (LAD) and then reperfusion for up to 30days.
  6. 06AnimalAnimal study (in vivo)Efficacy outcome

    In aged mice after myocardial infarction, AICAR improved apical end diastolic dimension, indicating reduced adverse remodeling.

    In plain wordsIn mice after a heart attack, AICAR improved apical end diastolic dimension, a measure of heart remodeling.

    Peptide
    AICAR (acadesine)
    Outcome
    Direction not reportedApical end diastolic dimension
    Study

    mousen: not reported in source

    Aged mice with reperfused myocardial infarction
    Outcome group
    Heart function · Cardiovascular
    Studied dose
    Dose not stated · injectionAs given in this study (mouse).

    Source sentences

    Summary
    The AICAR-treated group has demonstrated reduced adverse remodeling as indicated by improved apical end diastolic dimension but no changes in ejection fraction and cardiac output were observed.
    1 context sentence
    Summary · context
    In the present study, we injected aged mice with AICAR and subjected them to 1h occlusion of the left anterior descending artery (LAD) and then reperfusion for up to 30days.
  7. 07AnimalAnimal study (in vivo)Efficacy outcome

    In aged mice after myocardial infarction, AICAR did not change ejection fraction.

    In plain wordsIn mice after a heart attack, AICAR did not change ejection fraction.

    Peptide
    AICAR (acadesine)
    Outcome
    No significant changeEjection fraction
    Study

    mousen: not reported in source

    Aged mice with reperfused myocardial infarction
    Outcome group
    Heart function · Cardiovascular
    Studied dose
    Dose not stated · injectionAs given in this study (mouse).

    Source sentences

    Summary
    The AICAR-treated group has demonstrated reduced adverse remodeling as indicated by improved apical end diastolic dimension but no changes in ejection fraction and cardiac output were observed.
    1 context sentence
    Summary · context
    In the present study, we injected aged mice with AICAR and subjected them to 1h occlusion of the left anterior descending artery (LAD) and then reperfusion for up to 30days.
  8. 08AnimalAnimal study (in vivo)Efficacy outcome

    In aged mice after myocardial infarction, AICAR did not change cardiac output.

    In plain wordsIn mice after a heart attack, AICAR did not change cardiac output.

    Peptide
    AICAR (acadesine)
    Outcome
    No significant changeCardiac output
    Study

    mousen: not reported in source

    Aged mice with reperfused myocardial infarction
    Outcome group
    Heart function · Cardiovascular
    Studied dose
    Dose not stated · injectionAs given in this study (mouse).

    Source sentences

    Summary
    The AICAR-treated group has demonstrated reduced adverse remodeling as indicated by improved apical end diastolic dimension but no changes in ejection fraction and cardiac output were observed.
    1 context sentence
    Summary · context
    In the present study, we injected aged mice with AICAR and subjected them to 1h occlusion of the left anterior descending artery (LAD) and then reperfusion for up to 30days.

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.

PepBank is a research reference. Talk to a doctor before you use any peptide.