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Study · Animal study (in vivo) · mouse · 2010

19 results

Adenosine monophosphate-activated protein kinase induces cholesterol efflux from macrophage-derived foam cells and alleviates atherosclerosis in apolipoprotein E-deficient mice.

Li D, Wang D, Wang Y, Ling W, Feng X, Xia M

The Journal of biological chemistry16 Aug 2010Cited by 98 (Europe PMC)

PMID20713354 (opens in a new tab)PMCIDPMC2963409 (opens in a new tab)DOI10.1074/jbc.m110.159772 (opens in a new tab)PepBankPUB-20713354
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Summary

Increasing evidence suggests that adenosine monophosphate-activated protein kinase (AMPK) exerts protective effects for cardiovascular diseases apart from the regulation of energy homeostasis. However, the role of AMPK and its underlying mechanism on macrophage foam cell formation are poorly understood. In this study, we sought to investigate the potential effects of AMPK in modulating cholesterol deposition by using murine macrophage-derived foam cells. Incubation with 5-aminoimidazole-4-carboxyamide ribonucleoside (AICAR) markedly attenuated the cholesterol ester accumulation in oxidized low density lipoprotein-loaded macrophages. Notably, AICAR treatment significantly increased ATP-binding cassette transporters G1 (Abcg1) mRNA and protein levels without affecting mRNA and protein expression of ABCA1, scavenger receptors, including scavenger receptor-A, CD36, and scavenger receptor-BI (SR-BI), and cholesterol synthesis-related genes. The up-regulation of Abcg1 by AICAR was independent of the liver X receptor/retinoid X receptor pathway but dependent on ERK activation. AICAR elevates Abcg1 expression through a post-transcriptional mechanism that stabilizes the mRNA. Using a heterologous system with luciferase as a reporter, we further identify the Abcg1 mRNA 3'-UTR responsible for the regulatory effect of AICAR. Prevention of ABCG1 expression by small interfering RNA abolished the AICAR-mediated attenuation on foam cell formation. Furthermore, increased ABCG1 expression and reduced lipid accumulation were demonstrated in AICAR-treated macrophages isolated from apolipoprotein E-deficient mice (apoE(-/-) mice). AICAR treatment also inhibited atherosclerotic plaque formation in apoE(-/-) mice. Our findings elucidate a precise mechanism involved in the prevention of atherogenesis by AMPK.
CC BYText from Europe PMC. Highlighted sentences are the source of results.

Results from this study19

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

  1. 01AnimalAnimal study (in vivo)Mechanism

    In apoE-deficient mice, AICAR inhibited atherosclerotic plaque formation.

    In plain wordsIn apoE-deficient mice, AICAR reduced atherosclerotic plaque formation.

    Peptide
    AICAR (acadesine)
    Outcome
    DecreaseAtherosclerotic plaque formation
    Study

    mousen: not reported in source

    ApoE-deficient mice
    Outcome group
    Lipids · Cardiovascular
    Studied dose
    Dose not stated

    Source sentences

    Summary
    AICAR treatment also inhibited atherosclerotic plaque formation in apoE(-/-) mice.
  2. 02LabEx vivo tissueMechanism

    In macrophages isolated from apoE-deficient mice, AICAR treatment increased ABCG1 expression.

    In plain wordsIn lab tests on macrophages from apoE-deficient mice, AICAR increased ABCG1 expression.

    Peptide
    AICAR (acadesine)
    Outcome
    IncreaseABCG1 expression in isolated macrophages
    Study

    mousen: not reported in source

    Macrophages isolated from apoE-deficient mice
    Outcome group
    Lipids · Cardiovascular
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Furthermore, increased ABCG1 expression and reduced lipid accumulation were demonstrated in AICAR-treated macrophages isolated from apolipoprotein E-deficient mice (apoE(-/-) mice).
  3. 03LabEx vivo tissueMechanism

    In macrophages isolated from apoE-deficient mice, AICAR treatment reduced lipid accumulation.

    In plain wordsIn lab tests on macrophages from apoE-deficient mice, AICAR reduced lipid accumulation.

    Peptide
    AICAR (acadesine)
    Outcome
    DecreaseLipid accumulation in isolated macrophages
    Study

    mousen: not reported in source

    Macrophages isolated from apoE-deficient mice
    Outcome group
    Lipids · Cardiovascular
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Furthermore, increased ABCG1 expression and reduced lipid accumulation were demonstrated in AICAR-treated macrophages isolated from apolipoprotein E-deficient mice (apoE(-/-) mice).
  4. 04LabIn vitro (cells)Mechanism

    In oxidized LDL-loaded murine macrophages, AICAR attenuated cholesterol ester accumulation.

    In plain wordsIn cells from mice, AICAR reduced cholesterol ester accumulation during exposure to oxidized LDL.

    Peptide
    AICAR (acadesine)
    Outcome
    DecreaseCholesterol ester accumulation
    Study

    mousen: not reported in source

    Murine macrophage-derived foam cells
    Outcome group
    Lipids · Cardiovascular
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Incubation with 5-aminoimidazole-4-carboxyamide ribonucleoside (AICAR) markedly attenuated the cholesterol ester accumulation in oxidized low density lipoprotein-loaded macrophages.
  5. 05LabIn vitro (cells)Mechanism

    In murine macrophages, AICAR increased Abcg1 mRNA levels.

    In plain wordsIn cells from mice, AICAR increased Abcg1 gene expression.

    Peptide
    AICAR (acadesine)
    Outcome
    IncreaseAbcg1 mRNA
    Study

    mousen: not reported in source

    Murine macrophage-derived foam cells
    Outcome group
    Lipids · Cardiovascular
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Notably, AICAR treatment significantly increased ATP-binding cassette transporters G1 (Abcg1) mRNA and protein levels
  6. 06LabIn vitro (cells)Mechanism

    In murine macrophages, AICAR increased Abcg1 protein levels.

    In plain wordsIn cells from mice, AICAR increased Abcg1 protein.

    Peptide
    AICAR (acadesine)
    Outcome
    IncreaseAbcg1 protein
    Study

    mousen: not reported in source

    Murine macrophage-derived foam cells
    Outcome group
    Lipids · Cardiovascular
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Notably, AICAR treatment significantly increased ATP-binding cassette transporters G1 (Abcg1) mRNA and protein levels
  7. 07LabIn vitro (cells)Mechanism

    In murine macrophages, AICAR did not affect ABCA1 mRNA expression.

    In plain wordsIn cells from mice, AICAR did not change ABCA1 gene expression.

    Peptide
    AICAR (acadesine)
    Outcome
    No significant changeABCA1 mRNA
    Study

    mousen: not reported in source

    Murine macrophage-derived foam cells
    Outcome group
    Lipids · Cardiovascular
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Notably, AICAR treatment significantly increased ATP-binding cassette transporters G1 (Abcg1) mRNA and protein levels without affecting mRNA and protein expression of ABCA1, scavenger receptors, including scavenger receptor-A, CD36, and scavenger receptor-BI (SR-BI), and cholesterol synthesis-related genes.
  8. 08LabIn vitro (cells)Mechanism

    In murine macrophages, AICAR did not affect ABCA1 protein expression.

    In plain wordsIn cells from mice, AICAR did not change ABCA1 protein expression.

    Peptide
    AICAR (acadesine)
    Outcome
    No significant changeABCA1 protein
    Study

    mousen: not reported in source

    Murine macrophage-derived foam cells
    Outcome group
    Lipids · Cardiovascular
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Notably, AICAR treatment significantly increased ATP-binding cassette transporters G1 (Abcg1) mRNA and protein levels without affecting mRNA and protein expression of ABCA1, scavenger receptors, including scavenger receptor-A, CD36, and scavenger receptor-BI (SR-BI), and cholesterol synthesis-related genes.
  9. 09LabIn vitro (cells)Mechanism

    In murine macrophages, AICAR did not affect scavenger receptor-A mRNA expression.

    In plain wordsIn cells from mice, AICAR did not change scavenger receptor-A gene expression.

    Peptide
    AICAR (acadesine)
    Outcome
    No significant changeScavenger receptor-A mRNA
    Study

    mousen: not reported in source

    Murine macrophage-derived foam cells
    Outcome group
    Lipids · Cardiovascular
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Notably, AICAR treatment significantly increased ATP-binding cassette transporters G1 (Abcg1) mRNA and protein levels without affecting mRNA and protein expression of ABCA1, scavenger receptors, including scavenger receptor-A, CD36, and scavenger receptor-BI (SR-BI), and cholesterol synthesis-related genes.
  10. 10LabIn vitro (cells)Mechanism

    In murine macrophages, AICAR did not affect scavenger receptor-A protein expression.

    In plain wordsIn cells from mice, AICAR did not change scavenger receptor-A protein expression.

    Peptide
    AICAR (acadesine)
    Outcome
    No significant changeScavenger receptor-A protein
    Study

    mousen: not reported in source

    Murine macrophage-derived foam cells
    Outcome group
    Lipids · Cardiovascular
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Notably, AICAR treatment significantly increased ATP-binding cassette transporters G1 (Abcg1) mRNA and protein levels without affecting mRNA and protein expression of ABCA1, scavenger receptors, including scavenger receptor-A, CD36, and scavenger receptor-BI (SR-BI), and cholesterol synthesis-related genes.
  11. 11LabIn vitro (cells)Mechanism

    In murine macrophages, AICAR did not affect CD36 mRNA expression.

    In plain wordsIn cells from mice, AICAR did not change CD36 gene expression.

    Peptide
    AICAR (acadesine)
    Outcome
    No significant changeCD36 mRNA
    Study

    mousen: not reported in source

    Murine macrophage-derived foam cells
    Outcome group
    Lipids · Cardiovascular
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Notably, AICAR treatment significantly increased ATP-binding cassette transporters G1 (Abcg1) mRNA and protein levels without affecting mRNA and protein expression of ABCA1, scavenger receptors, including scavenger receptor-A, CD36, and scavenger receptor-BI (SR-BI), and cholesterol synthesis-related genes.
  12. 12LabIn vitro (cells)Mechanism

    In murine macrophages, AICAR did not affect CD36 protein expression.

    In plain wordsIn cells from mice, AICAR did not change CD36 protein expression.

    Peptide
    AICAR (acadesine)
    Outcome
    No significant changeCD36 protein
    Study

    mousen: not reported in source

    Murine macrophage-derived foam cells
    Outcome group
    Lipids · Cardiovascular
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Notably, AICAR treatment significantly increased ATP-binding cassette transporters G1 (Abcg1) mRNA and protein levels without affecting mRNA and protein expression of ABCA1, scavenger receptors, including scavenger receptor-A, CD36, and scavenger receptor-BI (SR-BI), and cholesterol synthesis-related genes.
  13. 13LabIn vitro (cells)Mechanism

    In murine macrophages, AICAR did not affect SR-BI mRNA expression.

    In plain wordsIn cells from mice, AICAR did not change SR-BI gene expression.

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

    mousen: not reported in source

    Murine macrophage-derived foam cells
    Outcome group
    Lipids · Cardiovascular
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Notably, AICAR treatment significantly increased ATP-binding cassette transporters G1 (Abcg1) mRNA and protein levels without affecting mRNA and protein expression of ABCA1, scavenger receptors, including scavenger receptor-A, CD36, and scavenger receptor-BI (SR-BI), and cholesterol synthesis-related genes.
  14. 14LabIn vitro (cells)Mechanism

    In murine macrophages, AICAR did not affect SR-BI protein expression.

    In plain wordsIn cells from mice, AICAR did not change SR-BI protein expression.

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

    mousen: not reported in source

    Murine macrophage-derived foam cells
    Outcome group
    Lipids · Cardiovascular
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Notably, AICAR treatment significantly increased ATP-binding cassette transporters G1 (Abcg1) mRNA and protein levels without affecting mRNA and protein expression of ABCA1, scavenger receptors, including scavenger receptor-A, CD36, and scavenger receptor-BI (SR-BI), and cholesterol synthesis-related genes.
  15. 15LabIn vitro (cells)Mechanism

    In murine macrophages, AICAR did not affect cholesterol synthesis-related gene expression.

    In plain wordsIn cells from mice, AICAR did not change expression of genes related to cholesterol synthesis.

    Peptide
    AICAR (acadesine)
    Outcome
    No significant changeCholesterol synthesis-related gene expression
    Study

    mousen: not reported in source

    Murine macrophage-derived foam cells
    Outcome group
    Lipids · Cardiovascular
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Notably, AICAR treatment significantly increased ATP-binding cassette transporters G1 (Abcg1) mRNA and protein levels without affecting mRNA and protein expression of ABCA1, scavenger receptors, including scavenger receptor-A, CD36, and scavenger receptor-BI (SR-BI), and cholesterol synthesis-related genes.
  16. 16LabIn vitro (cells)Mechanism

    In murine macrophages, AICAR-induced Abcg1 upregulation depended on ERK activation and was independent of the liver X receptor/retinoid X receptor pathway.

    In plain wordsIn cells from mice, AICAR regulation of Abcg1 required ERK but did not require the liver X receptor/retinoid X receptor pathway.

    Peptide
    AICAR (acadesine)
    Outcome
    Not applicableERK-dependent Abcg1 upregulation
    Study

    mousen: not reported in source

    Murine macrophage-derived foam cells
    Outcome group
    Lipids · Cardiovascular
    Studied dose
    Dose not stated

    Source sentences

    Summary
    The up-regulation of Abcg1 by AICAR was independent of the liver X receptor/retinoid X receptor pathway but dependent on ERK activation.
  17. 17LabIn vitro (cells)Mechanism

    In murine macrophages, AICAR increased Abcg1 expression through post-transcriptional mRNA stabilization.

    In plain wordsIn cells from mice, AICAR increased Abcg1 expression by stabilizing its mRNA.

    Peptide
    AICAR (acadesine)
    Outcome
    IncreaseAbcg1 mRNA stabilization
    Study

    mousen: not reported in source

    Murine macrophage-derived foam cells
    Outcome group
    Lipids · Cardiovascular
    Studied dose
    Dose not stated

    Source sentences

    Summary
    AICAR elevates Abcg1 expression through a post-transcriptional mechanism that stabilizes the mRNA.
  18. 18LabIn vitro (cells)Mechanism

    In a heterologous reporter system, the Abcg1 mRNA 3'-UTR mediated the regulatory effect of AICAR.

    In plain wordsIn lab tests, the Abcg1 mRNA 3'-UTR mediated regulation by AICAR.

    Peptide
    AICAR (acadesine)
    Outcome
    Not applicableAbcg1 mRNA regulatory region
    Study

    n: not reported in source

    Heterologous luciferase reporter system
    Outcome group
    Lipids · Cardiovascular
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Using a heterologous system with luciferase as a reporter, we further identify the Abcg1 mRNA 3'-UTR responsible for the regulatory effect of AICAR.

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. 19LabNot a test of AICAR (acadesine) aloneIn vitro (cells)Mechanism

    In murine macrophages, ABCG1 silencing abolished the attenuation of foam cell formation induced by AICAR.

    In plain wordsIn cells from mice, ABCG1 gene silencing blocked the reduction in foam cell formation induced by AICAR.

    Peptide
    AICAR (acadesine)
    Outcome
    IncreaseFoam cell formation after ABCG1 silencing
    Study

    mousen: not reported in source

    Murine macrophage-derived foam cells
    Outcome group
    Lipids · Cardiovascular

    Source sentences

    Summary
    Prevention of ABCG1 expression by small interfering RNA abolished the AICAR-mediated attenuation on foam cell formation.

    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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