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Study · Ex vivo tissue · rat · 2015

16 results

Pharmacological activation of AMPK prevents Drp1-mediated mitochondrial fission and alleviates endoplasmic reticulum stress-associated endothelial dysfunction.

Li J, Wang Y, Wang Y, Wen X, Ma XN, Chen W, Huang F, Kou J, Qi LW, Liu B, Liu K

Journal of molecular and cellular cardiology18 Jul 2015Cited by 165 (Europe PMC)

PMID26196303 (opens in a new tab)DOI10.1016/j.yjmcc.2015.07.010 (opens in a new tab)PepBankPUB-26196303
Publisher pagePubMedAsk about this study
Jump to 16 results

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 study16

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

  1. 01LabEx vivo tissueMechanism

    In rat aorta, AICAR enhanced eNOS phosphorylation.

    In plain wordsIn lab tests with rat aorta, AICAR increased eNOS phosphorylation.

    Peptide
    AICAR (acadesine)
    Outcome
    IncreaseeNOS phosphorylation
    Study

    ratn: not reported in source

    Rat aorta
    Outcome group
    Receptor activity and mechanism · Cardiovascular
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Meanwhile, salicylate and AICAR enhanced eNOS phosphorylation and restored the loss of endothelium-dependent vasodilation in the rat aorta.
    2 context sentences
    Summary · context
    Experimental approach Palmitate stimulation induced mitochondrial fission and ER stress-associated endothelial dysfunction.
    Summary · context
    The effects of AMPK activators salicylate and AICA riboside (AICAR) on mitochondrial ROS production, Drp1 phosphorylation, mitochondrial fission, ER stress, thioredoxin-interacting protein (TXNIP)/NLRP3 inflammasome activation, inflammation, cell apoptosis and endothelium-dependent vasodilation were observed.
  2. 02LabEx vivo tissueMechanism

    In rat aorta, AICAR restored impaired endothelium-dependent vasodilation.

    In plain wordsIn lab tests with rat aorta, AICAR restored blood-vessel relaxation controlled by its inner lining.

    Peptide
    AICAR (acadesine)
    Outcome
    IncreaseEndothelium-dependent vasodilation
    Study

    ratn: not reported in source

    Rat aorta
    Outcome group
    Receptor activity and mechanism · Cardiovascular
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Meanwhile, salicylate and AICAR enhanced eNOS phosphorylation and restored the loss of endothelium-dependent vasodilation in the rat aorta.
    2 context sentences
    Summary · context
    Experimental approach Palmitate stimulation induced mitochondrial fission and ER stress-associated endothelial dysfunction.
    Summary · context
    The effects of AMPK activators salicylate and AICA riboside (AICAR) on mitochondrial ROS production, Drp1 phosphorylation, mitochondrial fission, ER stress, thioredoxin-interacting protein (TXNIP)/NLRP3 inflammasome activation, inflammation, cell apoptosis and endothelium-dependent vasodilation were observed.
  3. 03LabIn vitro (cells)Mechanism

    In endothelial cells, AICAR prevented ROS-induced mitochondrial fission.

    In plain wordsIn cells, AICAR prevented mitochondrial splitting induced by reactive oxygen species.

    Peptide
    AICAR (acadesine)
    Outcome
    DecreaseMitochondrial fission
    Study

    n: not reported in source

    Palmitate-stimulated endothelial cells
    Outcome group
    Receptor activity and mechanism · Cardiovascular
    Studied dose
    Dose not stated

    Source sentences

    Summary
    AMPK activators salicylate and AICAR prevented ROS-induced mitochondrial fission by enhancing dynamin-related protein 1 (Drp1) phosphorylation (Ser 637) and thereby attenuated IRE-1α and PERK phosphorylation, but their actions were blocked by knockdown of AMPK.
    2 context sentences
    Summary · context
    Experimental approach Palmitate stimulation induced mitochondrial fission and ER stress-associated endothelial dysfunction.
    Summary · context
    The effects of AMPK activators salicylate and AICA riboside (AICAR) on mitochondrial ROS production, Drp1 phosphorylation, mitochondrial fission, ER stress, thioredoxin-interacting protein (TXNIP)/NLRP3 inflammasome activation, inflammation, cell apoptosis and endothelium-dependent vasodilation were observed.
  4. 04LabIn vitro (cells)Mechanism

    In endothelial cells, AICAR enhanced Drp1 phosphorylation at Ser 637.

    In plain wordsIn cells, AICAR increased Drp1 phosphorylation at Ser 637.

    Peptide
    AICAR (acadesine)
    Outcome
    IncreaseDrp1 Ser 637 phosphorylation
    Study

    n: not reported in source

    Palmitate-stimulated endothelial cells
    Outcome group
    Receptor activity and mechanism · Cardiovascular
    Studied dose
    Dose not stated

    Source sentences

    Summary
    AMPK activators salicylate and AICAR prevented ROS-induced mitochondrial fission by enhancing dynamin-related protein 1 (Drp1) phosphorylation (Ser 637) and thereby attenuated IRE-1α and PERK phosphorylation, but their actions were blocked by knockdown of AMPK.
    2 context sentences
    Summary · context
    Experimental approach Palmitate stimulation induced mitochondrial fission and ER stress-associated endothelial dysfunction.
    Summary · context
    The effects of AMPK activators salicylate and AICA riboside (AICAR) on mitochondrial ROS production, Drp1 phosphorylation, mitochondrial fission, ER stress, thioredoxin-interacting protein (TXNIP)/NLRP3 inflammasome activation, inflammation, cell apoptosis and endothelium-dependent vasodilation were observed.
  5. 05LabIn vitro (cells)Mechanism

    In endothelial cells, AICAR attenuated IRE-1α phosphorylation.

    In plain wordsIn cells, AICAR reduced IRE-1α phosphorylation.

    Peptide
    AICAR (acadesine)
    Outcome
    DecreaseIRE-1α phosphorylation
    Study

    n: not reported in source

    Palmitate-stimulated endothelial cells
    Outcome group
    Receptor activity and mechanism · Cardiovascular
    Studied dose
    Dose not stated

    Source sentences

    Summary
    AMPK activators salicylate and AICAR prevented ROS-induced mitochondrial fission by enhancing dynamin-related protein 1 (Drp1) phosphorylation (Ser 637) and thereby attenuated IRE-1α and PERK phosphorylation, but their actions were blocked by knockdown of AMPK.
    2 context sentences
    Summary · context
    Experimental approach Palmitate stimulation induced mitochondrial fission and ER stress-associated endothelial dysfunction.
    Summary · context
    The effects of AMPK activators salicylate and AICA riboside (AICAR) on mitochondrial ROS production, Drp1 phosphorylation, mitochondrial fission, ER stress, thioredoxin-interacting protein (TXNIP)/NLRP3 inflammasome activation, inflammation, cell apoptosis and endothelium-dependent vasodilation were observed.
  6. 06LabIn vitro (cells)Mechanism

    In endothelial cells, AICAR attenuated PERK phosphorylation.

    In plain wordsIn cells, AICAR reduced PERK phosphorylation.

    Peptide
    AICAR (acadesine)
    Outcome
    DecreasePERK phosphorylation
    Study

    n: not reported in source

    Palmitate-stimulated endothelial cells
    Outcome group
    Receptor activity and mechanism · Cardiovascular
    Studied dose
    Dose not stated

    Source sentences

    Summary
    AMPK activators salicylate and AICAR prevented ROS-induced mitochondrial fission by enhancing dynamin-related protein 1 (Drp1) phosphorylation (Ser 637) and thereby attenuated IRE-1α and PERK phosphorylation, but their actions were blocked by knockdown of AMPK.
    2 context sentences
    Summary · context
    Experimental approach Palmitate stimulation induced mitochondrial fission and ER stress-associated endothelial dysfunction.
    Summary · context
    The effects of AMPK activators salicylate and AICA riboside (AICAR) on mitochondrial ROS production, Drp1 phosphorylation, mitochondrial fission, ER stress, thioredoxin-interacting protein (TXNIP)/NLRP3 inflammasome activation, inflammation, cell apoptosis and endothelium-dependent vasodilation were observed.
  7. 07LabIn vitro (cells)Mechanism

    In endothelial cells, AICAR reduced TXNIP induction.

    In plain wordsIn cells, AICAR reduced TXNIP induction.

    Peptide
    AICAR (acadesine)
    Outcome
    DecreaseTXNIP induction
    Study

    n: not reported in source

    Palmitate-stimulated endothelial cells
    Outcome group
    Receptor activity and mechanism · Cardiovascular
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Salicylate and AICAR reduced TXNIP induction and inhibited NLRP3 inflammasome activation by reducing NLRP3 and caspase-1 expression, leading to a reduction in IL-1β secretion.
    2 context sentences
    Summary · context
    Experimental approach Palmitate stimulation induced mitochondrial fission and ER stress-associated endothelial dysfunction.
    Summary · context
    The effects of AMPK activators salicylate and AICA riboside (AICAR) on mitochondrial ROS production, Drp1 phosphorylation, mitochondrial fission, ER stress, thioredoxin-interacting protein (TXNIP)/NLRP3 inflammasome activation, inflammation, cell apoptosis and endothelium-dependent vasodilation were observed.
  8. 08LabIn vitro (cells)Mechanism

    In endothelial cells, AICAR inhibited NLRP3 inflammasome activation.

    In plain wordsIn cells, AICAR reduced activation of an inflammatory protein complex.

    Peptide
    AICAR (acadesine)
    Outcome
    DecreaseNLRP3 inflammasome activation
    Study

    n: not reported in source

    Palmitate-stimulated endothelial cells
    Outcome group
    Receptor activity and mechanism · Cardiovascular
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Salicylate and AICAR reduced TXNIP induction and inhibited NLRP3 inflammasome activation by reducing NLRP3 and caspase-1 expression, leading to a reduction in IL-1β secretion.
    2 context sentences
    Summary · context
    Experimental approach Palmitate stimulation induced mitochondrial fission and ER stress-associated endothelial dysfunction.
    Summary · context
    The effects of AMPK activators salicylate and AICA riboside (AICAR) on mitochondrial ROS production, Drp1 phosphorylation, mitochondrial fission, ER stress, thioredoxin-interacting protein (TXNIP)/NLRP3 inflammasome activation, inflammation, cell apoptosis and endothelium-dependent vasodilation were observed.
  9. 09LabIn vitro (cells)Mechanism

    In endothelial cells, AICAR reduced NLRP3 expression.

    In plain wordsIn cells, AICAR reduced NLRP3 expression.

    Peptide
    AICAR (acadesine)
    Outcome
    DecreaseNLRP3 expression
    Study

    n: not reported in source

    Palmitate-stimulated endothelial cells
    Outcome group
    Receptor activity and mechanism · Cardiovascular
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Salicylate and AICAR reduced TXNIP induction and inhibited NLRP3 inflammasome activation by reducing NLRP3 and caspase-1 expression, leading to a reduction in IL-1β secretion.
    2 context sentences
    Summary · context
    Experimental approach Palmitate stimulation induced mitochondrial fission and ER stress-associated endothelial dysfunction.
    Summary · context
    The effects of AMPK activators salicylate and AICA riboside (AICAR) on mitochondrial ROS production, Drp1 phosphorylation, mitochondrial fission, ER stress, thioredoxin-interacting protein (TXNIP)/NLRP3 inflammasome activation, inflammation, cell apoptosis and endothelium-dependent vasodilation were observed.
  10. 10LabIn vitro (cells)Mechanism

    In endothelial cells, AICAR reduced caspase-1 expression.

    In plain wordsIn cells, AICAR reduced caspase-1 expression.

    Peptide
    AICAR (acadesine)
    Outcome
    DecreaseCaspase-1 expression
    Study

    n: not reported in source

    Palmitate-stimulated endothelial cells
    Outcome group
    Receptor activity and mechanism · Cardiovascular
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Salicylate and AICAR reduced TXNIP induction and inhibited NLRP3 inflammasome activation by reducing NLRP3 and caspase-1 expression, leading to a reduction in IL-1β secretion.
    2 context sentences
    Summary · context
    Experimental approach Palmitate stimulation induced mitochondrial fission and ER stress-associated endothelial dysfunction.
    Summary · context
    The effects of AMPK activators salicylate and AICA riboside (AICAR) on mitochondrial ROS production, Drp1 phosphorylation, mitochondrial fission, ER stress, thioredoxin-interacting protein (TXNIP)/NLRP3 inflammasome activation, inflammation, cell apoptosis and endothelium-dependent vasodilation were observed.
  11. 11LabIn vitro (cells)Mechanism

    In endothelial cells, AICAR reduced IL-1β secretion.

    In plain wordsIn cells, AICAR reduced release of IL-1β.

    Peptide
    AICAR (acadesine)
    Outcome
    DecreaseIL-1β secretion
    Study

    n: not reported in source

    Palmitate-stimulated endothelial cells
    Outcome group
    Receptor activity and mechanism · Cardiovascular
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Salicylate and AICAR reduced TXNIP induction and inhibited NLRP3 inflammasome activation by reducing NLRP3 and caspase-1 expression, leading to a reduction in IL-1β secretion.
    2 context sentences
    Summary · context
    Experimental approach Palmitate stimulation induced mitochondrial fission and ER stress-associated endothelial dysfunction.
    Summary · context
    The effects of AMPK activators salicylate and AICA riboside (AICAR) on mitochondrial ROS production, Drp1 phosphorylation, mitochondrial fission, ER stress, thioredoxin-interacting protein (TXNIP)/NLRP3 inflammasome activation, inflammation, cell apoptosis and endothelium-dependent vasodilation were observed.
  12. 12LabIn vitro (cells)Mechanism

    In endothelial cells, AICAR inhibited inflammation.

    In plain wordsIn cells, AICAR reduced inflammation.

    Peptide
    AICAR (acadesine)
    Outcome
    DecreaseInflammation
    Study

    n: not reported in source

    Palmitate-stimulated endothelial cells
    Outcome group
    Receptor activity and mechanism · Cardiovascular
    Studied dose
    Dose not stated

    Source sentences

    Summary
    As a result, salicylate and AICAR inhibited inflammation and reduced cell apoptosis.
    2 context sentences
    Summary · context
    Experimental approach Palmitate stimulation induced mitochondrial fission and ER stress-associated endothelial dysfunction.
    Summary · context
    The effects of AMPK activators salicylate and AICA riboside (AICAR) on mitochondrial ROS production, Drp1 phosphorylation, mitochondrial fission, ER stress, thioredoxin-interacting protein (TXNIP)/NLRP3 inflammasome activation, inflammation, cell apoptosis and endothelium-dependent vasodilation were observed.
  13. 13LabIn vitro (cells)Mechanism

    In endothelial cells, AICAR reduced apoptosis.

    In plain wordsIn cells, AICAR reduced programmed cell death.

    Peptide
    AICAR (acadesine)
    Outcome
    DecreaseCell apoptosis
    Study

    n: not reported in source

    Palmitate-stimulated endothelial cells
    Outcome group
    Receptor activity and mechanism · Cardiovascular
    Studied dose
    Dose not stated

    Source sentences

    Summary
    As a result, salicylate and AICAR inhibited inflammation and reduced cell apoptosis.
    2 context sentences
    Summary · context
    Experimental approach Palmitate stimulation induced mitochondrial fission and ER stress-associated endothelial dysfunction.
    Summary · context
    The effects of AMPK activators salicylate and AICA riboside (AICAR) on mitochondrial ROS production, Drp1 phosphorylation, mitochondrial fission, ER stress, thioredoxin-interacting protein (TXNIP)/NLRP3 inflammasome activation, inflammation, cell apoptosis and endothelium-dependent vasodilation were observed.

Studies that did not test the peptide alone3

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. 14LabNot a test of AICAR (acadesine) aloneEx vivo tissueMechanism

    In vascular endothelium, pharmacological AMPK activation inhibited endoplasmic reticulum stress.

    In plain wordsIn lab tests, AMPK activation reduced stress in the endoplasmic reticulum of vessel-lining cells.

    Peptide
    AICAR (acadesine)
    Outcome
    DecreaseEndoplasmic reticulum stress
    Study

    n: not reported in source

    Vascular endothelium examined by immunohistochemistry
    Outcome group
    Receptor activity and mechanism · Cardiovascular

    Source sentences

    Summary
    Immunohistochemistry staining showed that AMPK activation inhibited ER stress and NLRP3 inflammasome activation in the vascular endothelium.
    2 context sentences
    Summary · context
    Experimental approach Palmitate stimulation induced mitochondrial fission and ER stress-associated endothelial dysfunction.
    Summary · context
    The effects of AMPK activators salicylate and AICA riboside (AICAR) on mitochondrial ROS production, Drp1 phosphorylation, mitochondrial fission, ER stress, thioredoxin-interacting protein (TXNIP)/NLRP3 inflammasome activation, inflammation, cell apoptosis and endothelium-dependent vasodilation were observed.

    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. 15LabNot a test of AICAR (acadesine) aloneEx vivo tissueMechanism

    In vascular endothelium, pharmacological AMPK activation inhibited NLRP3 inflammasome activation.

    In plain wordsIn lab tests, AMPK activation reduced activation of an inflammatory protein complex in vessel-lining cells.

    Peptide
    AICAR (acadesine)
    Outcome
    DecreaseVascular NLRP3 inflammasome activation
    Study

    n: not reported in source

    Vascular endothelium examined by immunohistochemistry
    Outcome group
    Receptor activity and mechanism · Cardiovascular

    Source sentences

    Summary
    Immunohistochemistry staining showed that AMPK activation inhibited ER stress and NLRP3 inflammasome activation in the vascular endothelium.
    2 context sentences
    Summary · context
    Experimental approach Palmitate stimulation induced mitochondrial fission and ER stress-associated endothelial dysfunction.
    Summary · context
    The effects of AMPK activators salicylate and AICA riboside (AICAR) on mitochondrial ROS production, Drp1 phosphorylation, mitochondrial fission, ER stress, thioredoxin-interacting protein (TXNIP)/NLRP3 inflammasome activation, inflammation, cell apoptosis and endothelium-dependent vasodilation were observed.

    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. 16LabNot a test of AICAR (acadesine) aloneIn vitro (cells)Mechanism

    In endothelial cells, AMPK knockdown blocked the reported actions of AICAR and salicylate.

    In plain wordsIn cells, reducing AMPK expression blocked the reported effects of AICAR and salicylate.

    Peptide
    AICAR (acadesine)
    Outcome
    Not applicableAMPK dependence of cellular effects
    Study

    n: not reported in source

    Palmitate-stimulated endothelial cells
    Outcome group
    Receptor activity and mechanism · Cardiovascular

    Source sentences

    Summary
    AMPK activators salicylate and AICAR prevented ROS-induced mitochondrial fission by enhancing dynamin-related protein 1 (Drp1) phosphorylation (Ser 637) and thereby attenuated IRE-1α and PERK phosphorylation, but their actions were blocked by knockdown of AMPK.
    2 context sentences
    Summary · context
    Experimental approach Palmitate stimulation induced mitochondrial fission and ER stress-associated endothelial dysfunction.
    Summary · context
    The effects of AMPK activators salicylate and AICA riboside (AICAR) on mitochondrial ROS production, Drp1 phosphorylation, mitochondrial fission, ER stress, thioredoxin-interacting protein (TXNIP)/NLRP3 inflammasome activation, inflammation, cell apoptosis and endothelium-dependent vasodilation were observed.

    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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