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Study · Animal study (in vivo) · mouse · 2025

3 results

AMPK phosphorylation of KCa2.3 alleviates angiotensin II-induced endothelial dysfunction.

Pang ZD, Wang Y, Han MZ, She G, Sun X, Bai RY, Lai BC, Zhang Y, Du XJ, Shyy JY, Deng XL

Biochemical pharmacology18 Mar 2025Cited by 3 (Europe PMC)

PMID40112931 (opens in a new tab)DOI10.1016/j.bcp.2025.116880 (opens in a new tab)PepBankPUB-40112931
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 study3

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

  1. 01AnimalAnimal study (in vivo)Mechanism

    In angiotensin II-infused mice, AICAR restored KCa2.3-mediated EDH-dependent mesenteric resistance artery relaxation.

    In plain wordsIn mice with angiotensin-induced hypertension, AICAR restored a small-artery relaxation response.

    Peptide
    AICAR (acadesine)
    Outcome
    IncreaseEDH-dependent arterial relaxation
    Study

    mousen: not reported in source

    Angiotensin II-infused mice
    Outcome group
    Receptor activity and mechanism · Cardiovascular
    Studied dose
    Dose not stated · 2 weeksAs given in this study (mouse).

    Source sentences

    Summary
    In mice with angiotensin II infusion, 2-week treatment with AICAR or overexpressing phosphomimetic mutant KCa2.3 Thr107D (mouse) restored KCa2.3-mediated EDH-dependent relaxation in mesenteric resistance arteries together with reversal of early phase hypertension.
  2. 02AnimalAnimal study (in vivo)Efficacy outcome

    In angiotensin II-infused mice, AICAR reversed early phase hypertension.

    In plain wordsIn mice with angiotensin-induced hypertension, AICAR reversed early high blood pressure.

    Peptide
    AICAR (acadesine)
    Outcome
    DecreaseEarly phase hypertension
    Study

    mousen: not reported in source

    Angiotensin II-infused mice
    Outcome group
    Blood pressure · Cardiovascular
    Studied dose
    Dose not stated · 2 weeksAs given in this study (mouse).

    Source sentences

    Summary
    In mice with angiotensin II infusion, 2-week treatment with AICAR or overexpressing phosphomimetic mutant KCa2.3 Thr107D (mouse) restored KCa2.3-mediated EDH-dependent relaxation in mesenteric resistance arteries together with reversal of early phase hypertension.
  3. 03LabIn vitro (cells)Mechanism

    In HUVECs, AMPK activators including AICAR significantly increased KCa2.3 Thr106 phosphorylation, which compound C antagonized.

    In plain wordsIn cells, AICAR was among AMPK activators that increased potassium channel phosphorylation, an effect opposed by compound C.

    Peptide
    AICAR (acadesine)
    Outcome
    IncreaseKCa2.3 Thr106 phosphorylation
    Study

    humann: not reported in source

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

    Source sentences

    Summary
    In HUVECs, treatment with activators of AMPK (AICAR, metformin, and MK-8722) significantly increased phosphorylation of KCa2.3 Thr106 (human), which was antagonized by AMPK inhibitor compound C.

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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