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Study · In vitro (cells) · 2016

13 results

AMP-activated protein kinase attenuates oxLDL uptake in macrophages through PP2A/NF-κB/LOX-1 pathway.

Chen B, Li J, Zhu H

Vascular pharmacology19 Aug 2015Cited by 54 (Europe PMC)

PMID26297684 (opens in a new tab)DOI10.1016/j.vph.2015.08.012 (opens in a new tab)PepBankPUB-26297684
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 study13

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

  1. 01LabIn vitro (cells)Activity measurement

    In macrophages, AICAR-induced AMPK activation decreased cholesterol uptake.

    In plain wordsIn cells, AICAR-induced AMPK activation reduced cholesterol uptake.

    Peptide
    AICAR (acadesine)
    Outcome
    DecreaseMacrophage cholesterol uptake
    Study

    n: not reported in source

    macrophages
    Outcome group
    Lipids · Cardiovascular
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Here we demonstrate that AMPK activation in response to IMM-H007 or AICAR resulted in a decrease in macrophage cholesterol uptake and thus inhibited foam cell formation in macrophages mediated by oxidized low-density lipoprotein (oxLDL).
  2. 02LabIn vitro (cells)Activity measurement

    In macrophages, AICAR-induced AMPK activation inhibited oxLDL-mediated foam cell formation.

    In plain wordsIn cells, AICAR-induced AMPK activation reduced foam cell formation.

    Peptide
    AICAR (acadesine)
    Outcome
    DecreaseFoam cell formation
    Study

    n: not reported in source

    macrophages
    Outcome group
    Lipids · Cardiovascular
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Here we demonstrate that AMPK activation in response to IMM-H007 or AICAR resulted in a decrease in macrophage cholesterol uptake and thus inhibited foam cell formation in macrophages mediated by oxidized low-density lipoprotein (oxLDL).

Studies that did not test the peptide alone11

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) aloneAnimal study (in vivo)Efficacy outcome

    In apolipoprotein E-deficient mice, pharmacological AMPK activation reduced atherosclerotic lesion size.

    In plain wordsIn mice lacking apolipoprotein E, pharmacological AMPK activation reduced atherosclerotic lesions.

    Peptide
    AICAR (acadesine)
    Outcome
    DecreaseAtherosclerotic lesion size
    Study

    mousen: not reported in source

    apolipoprotein E-deficient mice
    Outcome group
    Cardiovascular events · Cardiovascular

    Source sentences

    Summary
    In vivo, pharmacological AMPK activation reduced the lesion size of atherosclerosis and the expression of LOX-1 in aortas in apolipoprotein E-deficient mice.
    1 context sentence
    Summary · context
    Here we demonstrate that AMPK activation in response to IMM-H007 or AICAR resulted in a decrease in macrophage cholesterol uptake and thus inhibited foam cell formation in macrophages mediated by oxidized low-density lipoprotein (oxLDL).

    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).

  2. 04AnimalNot a test of AICAR (acadesine) aloneAnimal study (in vivo)Mechanism

    In apolipoprotein E-deficient mice, pharmacological AMPK activation reduced aortic LOX-1 expression.

    In plain wordsIn mice lacking apolipoprotein E, pharmacological AMPK activation reduced aortic LOX-1 expression.

    Peptide
    AICAR (acadesine)
    Outcome
    DecreaseAortic LOX-1 expression
    Study

    mousen: not reported in source

    apolipoprotein E-deficient mice
    Outcome group
    Receptor activity and mechanism · Cardiovascular

    Source sentences

    Summary
    In vivo, pharmacological AMPK activation reduced the lesion size of atherosclerosis and the expression of LOX-1 in aortas in apolipoprotein E-deficient mice.
    1 context sentence
    Summary · context
    Here we demonstrate that AMPK activation in response to IMM-H007 or AICAR resulted in a decrease in macrophage cholesterol uptake and thus inhibited foam cell formation in macrophages mediated by oxidized low-density lipoprotein (oxLDL).

    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).

  3. 05LabNot a test of AICAR (acadesine) aloneIn vitro (cells)Mechanism

    In macrophages, pharmacological AMPK activation decreased LOX-1 mRNA expression.

    In plain wordsIn cells, pharmacological AMPK activation reduced LOX-1 mRNA expression.

    Peptide
    AICAR (acadesine)
    Outcome
    DecreaseLOX-1 mRNA expression
    Study

    n: not reported in source

    macrophages
    Outcome group
    Receptor activity and mechanism · Cardiovascular

    Source sentences

    Summary
    This functional change was caused by a downregulation of mRNA and protein expression of LOX-1 but not other scavenger receptors, including scavenger receptor-A (SR-A), CD36 and scavenger receptor-BI (SR-BI).
    1 context sentence
    Summary · context
    Here we demonstrate that AMPK activation in response to IMM-H007 or AICAR resulted in a decrease in macrophage cholesterol uptake and thus inhibited foam cell formation in macrophages mediated by oxidized low-density lipoprotein (oxLDL).

    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).

  4. 06LabNot a test of AICAR (acadesine) aloneIn vitro (cells)Mechanism

    In macrophages, pharmacological AMPK activation decreased LOX-1 protein expression.

    In plain wordsIn cells, pharmacological AMPK activation reduced LOX-1 protein expression.

    Peptide
    AICAR (acadesine)
    Outcome
    DecreaseLOX-1 protein expression
    Study

    n: not reported in source

    macrophages
    Outcome group
    Receptor activity and mechanism · Cardiovascular

    Source sentences

    Summary
    This functional change was caused by a downregulation of mRNA and protein expression of LOX-1 but not other scavenger receptors, including scavenger receptor-A (SR-A), CD36 and scavenger receptor-BI (SR-BI).
    1 context sentence
    Summary · context
    Here we demonstrate that AMPK activation in response to IMM-H007 or AICAR resulted in a decrease in macrophage cholesterol uptake and thus inhibited foam cell formation in macrophages mediated by oxidized low-density lipoprotein (oxLDL).

    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).

  5. 07LabNot a test of AICAR (acadesine) aloneIn vitro (cells)Mechanism

    In macrophages, pharmacological AMPK activation did not decrease SR-A expression.

    In plain wordsIn cells, pharmacological AMPK activation did not reduce SR-A expression.

    Peptide
    AICAR (acadesine)
    Outcome
    No significant changeSR-A expression
    Study

    n: not reported in source

    macrophages
    Outcome group
    Receptor activity and mechanism · Cardiovascular

    Source sentences

    Summary
    This functional change was caused by a downregulation of mRNA and protein expression of LOX-1 but not other scavenger receptors, including scavenger receptor-A (SR-A), CD36 and scavenger receptor-BI (SR-BI).
    1 context sentence
    Summary · context
    Here we demonstrate that AMPK activation in response to IMM-H007 or AICAR resulted in a decrease in macrophage cholesterol uptake and thus inhibited foam cell formation in macrophages mediated by oxidized low-density lipoprotein (oxLDL).

    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).

  6. 08LabNot a test of AICAR (acadesine) aloneIn vitro (cells)Mechanism

    In macrophages, pharmacological AMPK activation did not decrease CD36 expression.

    In plain wordsIn cells, pharmacological AMPK activation did not reduce CD36 expression.

    Peptide
    AICAR (acadesine)
    Outcome
    No significant changeCD36 expression
    Study

    n: not reported in source

    macrophages
    Outcome group
    Receptor activity and mechanism · Cardiovascular

    Source sentences

    Summary
    This functional change was caused by a downregulation of mRNA and protein expression of LOX-1 but not other scavenger receptors, including scavenger receptor-A (SR-A), CD36 and scavenger receptor-BI (SR-BI).
    1 context sentence
    Summary · context
    Here we demonstrate that AMPK activation in response to IMM-H007 or AICAR resulted in a decrease in macrophage cholesterol uptake and thus inhibited foam cell formation in macrophages mediated by oxidized low-density lipoprotein (oxLDL).

    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).

  7. 09LabNot a test of AICAR (acadesine) aloneIn vitro (cells)Mechanism

    In macrophages, pharmacological AMPK activation did not decrease SR-BI expression.

    In plain wordsIn cells, pharmacological AMPK activation did not reduce SR-BI expression.

    Peptide
    AICAR (acadesine)
    Outcome
    No significant changeSR-BI expression
    Study

    n: not reported in source

    macrophages
    Outcome group
    Receptor activity and mechanism · Cardiovascular

    Source sentences

    Summary
    This functional change was caused by a downregulation of mRNA and protein expression of LOX-1 but not other scavenger receptors, including scavenger receptor-A (SR-A), CD36 and scavenger receptor-BI (SR-BI).
    1 context sentence
    Summary · context
    Here we demonstrate that AMPK activation in response to IMM-H007 or AICAR resulted in a decrease in macrophage cholesterol uptake and thus inhibited foam cell formation in macrophages mediated by oxidized low-density lipoprotein (oxLDL).

    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).

  8. 10LabNot a test of AICAR (acadesine) aloneIn vitro (cells)Mechanism

    In macrophages, AMPK activation decreased NF-κB phosphorylation.

    In plain wordsIn cells, AMPK activation reduced NF-κB phosphorylation.

    Peptide
    AICAR (acadesine)
    Outcome
    DecreaseNF-κB phosphorylation
    Study

    n: not reported in source

    macrophages
    Outcome group
    Receptor activity and mechanism · Cardiovascular

    Source sentences

    Summary
    The expression of LOX-1 was regulated by AMPK activation induced decreased phosphorylation of nuclear transcription factor NF-κB,
    1 context sentence
    Summary · context
    Here we demonstrate that AMPK activation in response to IMM-H007 or AICAR resulted in a decrease in macrophage cholesterol uptake and thus inhibited foam cell formation in macrophages mediated by oxidized low-density lipoprotein (oxLDL).

    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).

  9. 11LabNot a test of AICAR (acadesine) aloneIn vitro (cells)Mechanism

    In macrophages, pharmacological AMPK activation promoted PP2A activity.

    In plain wordsIn cells, pharmacological AMPK activation increased PP2A activity.

    Peptide
    AICAR (acadesine)
    Outcome
    IncreasePP2A activity
    Study

    n: not reported in source

    macrophages
    Outcome group
    Receptor activity and mechanism · Cardiovascular

    Source sentences

    Summary
    Moreover, pharmacological AMPK activation was shown to promote protein phosphatase 2A (PP2A) activity and the specific PP2A inhibitor, okadaic acid, could prevent the effects of IMM-H007 or AICAR on NF-κB and LOX-1.
    1 context sentence
    Summary · context
    Here we demonstrate that AMPK activation in response to IMM-H007 or AICAR resulted in a decrease in macrophage cholesterol uptake and thus inhibited foam cell formation in macrophages mediated by oxidized low-density lipoprotein (oxLDL).

    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).

  10. 12LabNot a test of AICAR (acadesine) aloneIn vitro (cells)Mechanism

    In macrophages, okadaic acid prevented effects of IMM-H007 or AICAR on NF-κB.

    In plain wordsIn cells, okadaic acid blocked effects of IMM-H007 or AICAR on NF-κB.

    Peptide
    AICAR (acadesine)
    Outcome
    Not applicableOkadaic acid blockade of NF-κB effects
    Study

    n: not reported in source

    macrophages
    Outcome group
    Receptor activity and mechanism · Cardiovascular

    Source sentences

    Summary
    Moreover, pharmacological AMPK activation was shown to promote protein phosphatase 2A (PP2A) activity and the specific PP2A inhibitor, okadaic acid, could prevent the effects of IMM-H007 or AICAR on NF-κB and LOX-1.

    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).

  11. 13LabNot a test of AICAR (acadesine) aloneIn vitro (cells)Mechanism

    In macrophages, okadaic acid prevented effects of IMM-H007 or AICAR on LOX-1.

    In plain wordsIn cells, okadaic acid blocked effects of IMM-H007 or AICAR on LOX-1.

    Peptide
    AICAR (acadesine)
    Outcome
    Not applicableOkadaic acid blockade of LOX-1 effects
    Study

    n: not reported in source

    macrophages
    Outcome group
    Receptor activity and mechanism · Cardiovascular

    Source sentences

    Summary
    Moreover, pharmacological AMPK activation was shown to promote protein phosphatase 2A (PP2A) activity and the specific PP2A inhibitor, okadaic acid, could prevent the effects of IMM-H007 or AICAR on NF-κB and LOX-1.

    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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