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Study · In vitro (cells) · 2025

1 result

Adenylate kinase 4 (AK4) deficiency prevents vascular smooth muscle cell phenotypic switching by regulating mitochondrial dysfunction through AMPKα inactivation.

Zhang SM, Luo H, Li Z, Du M, Chen J, Jiang DS, Zhang Y, Li C, Yang X, Wang XS, Fang ZM, Gong FH, Yang J

Atherosclerosis4 Jun 2025Cited by 2 (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 aortic VSMCs, AICAR-mediated AMPK activation reversed the inhibitory effects of AK4 deficiency on phenotypic switching.

    In plain wordsIn cells, AICAR reversed suppression of phenotype changes compared with AK4 deficiency without AMPK activation.

    Outcome
    IncreaseHASMC phenotypic switching
    Study

    humann: not reported in source

    AK4-deficient human aortic vascular smooth muscle cells
    Comparator
    AK4 deficiency without AMPK activation
    Outcome group
    Receptor activity and mechanism · Cardiovascular
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Furthermore, activation of AMPKα by metformin or AICAR (acadesine) reversed the inhibitory effects of AK4 deficiency on HASMC phenotypic switching.

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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