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Study · In vitro (cells) · 2011

1 result

Chronic activation of AMP-activated protein kinase prevents 20-hydroxyeicosatetraenoic acid-induced endothelial dysfunction.

Ward NC, Chen K, Li C, Croft KD, Keaney JF Jr

Clinical and experimental pharmacology & physiology1 May 2011Cited by 17 (Europe PMC)

Summary

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Text rights: Publisher copyright. Results still quote short attributed sentences.

Results from this study1

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

  1. 01LabIn vitro (cells)Mechanism

    In human endothelial cells, AICAR pretreatment prevented the loss of Hsp90 association with eNOS after 20-HETE treatment.

    In plain wordsIn cells, AICAR pretreatment preserved Hsp90 binding to eNOS compared with 20-HETE treatment without pretreatment.

    Outcome
    IncreaseHsp90 association with eNOS
    Study

    humann: not reported in source

    Human umbilical vein endothelial cells
    Comparator
    20-HETE treatment without AICAR pretreatment
    Outcome group
    Receptor activity and mechanism · Cardiovascular
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Pretreatment of cells with 5'-aminoimidazole-4-carboxyamide-ribonucleoside (AICAR; a chronic activator of AMPK) prevented the loss of Hsp90 association with eNOS following 20-HETE treatment.
    1 context sentence
    Summary · context
    Immunoprecipitation of eNOS in human umbilical vein endothelial cells treated with 20-HETE

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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