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Study · In vitro (cells) · 2021

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Imatinib protects against human beta-cell death via inhibition of mitochondrial respiration and activation of AMPK.

Elksnis A, Schiffer TA, Palm F, Wang Y, Cen J, Turpaev K, Ngamjariyawat A, Younis S, Huang S, Shen Y, Leng Y, Bergsten P, Karlsborn T, Welsh N, Wang X

Clinical science (London, England : 1979)1 Oct 2021Cited by 9 (Europe PMC)

PMID34569605 (opens in a new tab)DOI10.1042/cs20210604 (opens in a new tab)PepBankPUB-34569605
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Summary

The protein tyrosine kinase inhibitor imatinib is used in the treatment of various malignancies but may also promote beneficial effects in the treatment of diabetes. The aim of the present investigation was to characterize the mechanisms by which imatinib protects insulin producing cells. Treatment of non-obese diabetic (NOD) mice with imatinib resulted in increased beta-cell AMP-activated kinase (AMPK) phosphorylation. Imatinib activated AMPK also in vitro, resulting in decreased ribosomal protein S6 phosphorylation and protection against islet amyloid polypeptide (IAPP)-aggregation, thioredoxin interacting protein (TXNIP) up-regulation and beta-cell death. 5-Aminoimidazole-4-carboxamide ribonucleotide (AICAR) mimicked and compound C counteracted the effect of imatinib on beta-cell survival. Imatinib-induced AMPK activation was preceded by reduced glucose/pyruvate-dependent respiration, increased glycolysis rates, and a lowered ATP/AMP ratio. Imatinib augmented the fractional oxidation of fatty acids/malate, possibly via a direct interaction with the beta-oxidation enzyme enoyl coenzyme A hydratase, short chain, 1, mitochondrial (ECHS1). In non-beta cells, imatinib reduced respiratory chain complex I and II-mediated respiration and acyl-CoA carboxylase (ACC) phosphorylation, suggesting that mitochondrial effects of imatinib are not beta-cell specific. In conclusion, tyrosine kinase inhibitors modestly inhibit mitochondrial respiration, leading to AMPK activation and TXNIP down-regulation, which in turn protects against beta-cell death.
CC BYText from Europe PMC. Highlighted sentences are the source of results.

Results from this study1

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

  1. 01LabIn vitro (cells)Efficacy outcome

    In beta cells, AICAR mimicked imatinib's protective effect on survival.

    In plain wordsIn cells, AICAR mimicked imatinib's protection of insulin-producing cells.

    Peptide
    AICAR (acadesine)
    Outcome
    IncreaseBeta-cell survival
    Study

    n: not reported in source

    beta cells
    Outcome group
    Cell viability and death · Metabolic and weight
    Studied dose
    Dose not stated

    Source sentences

    Summary
    5-Aminoimidazole-4-carboxamide ribonucleotide (AICAR) mimicked and compound C counteracted the effect of imatinib on beta-cell survival.

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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