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Study · Other design · 2026

3 results

GPR75 knockdown alleviates mitochondrial dysfunction in retinal ganglion cells via AMPK pathway in diabetic mice.

Liu M, Cheng X, Liu W, Yu H, Yu S, Wang Y, Chen X, Miao Q, Yuan Y, Dai W, Hu J, Zhang N, Sui J, Liu X, Zuo Z

Biochemical pharmacology15 Jul 2026

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. 01AnimalOther designMechanism

    In diabetic experimental models, AICAR mitigated GPR75-induced mitochondrial dysfunction.

    In plain wordsIn diabetic experimental models, AICAR reduced mitochondrial dysfunction induced by GPR75.

    Outcome
    DecreaseMitochondrial dysfunction
    Study

    n: not reported in source

    Diabetic mice and high-glucose-treated primary retinal ganglion cells
    Outcome group
    Neuroprotection · Eye
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Notably, the AMPK-activator AICAR mitigates GPR75-induced mitochondrial dysfunction, pyroptosis, and apoptosis.
    1 context sentence
    Summary · context
    To investigate the function of GPR75, we knockdown the receptor in streptozotocin (STZ) mice and high glucose (HG)-treated primary RGCs.
  2. 02AnimalOther designMechanism

    In diabetic experimental models, AICAR mitigated GPR75-induced pyroptosis.

    In plain wordsIn diabetic experimental models, AICAR reduced inflammatory cell death induced by GPR75.

    Outcome
    DecreasePyroptosis
    Study

    n: not reported in source

    Diabetic mice and high-glucose-treated primary retinal ganglion cells
    Outcome group
    Neuroprotection · Eye
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Notably, the AMPK-activator AICAR mitigates GPR75-induced mitochondrial dysfunction, pyroptosis, and apoptosis.
    1 context sentence
    Summary · context
    To investigate the function of GPR75, we knockdown the receptor in streptozotocin (STZ) mice and high glucose (HG)-treated primary RGCs.
  3. 03AnimalOther designMechanism

    In diabetic experimental models, AICAR mitigated GPR75-induced apoptosis.

    In plain wordsIn diabetic experimental models, AICAR reduced apoptosis induced by GPR75.

    Outcome
    DecreaseApoptosis
    Study

    n: not reported in source

    Diabetic mice and high-glucose-treated primary retinal ganglion cells
    Outcome group
    Neuroprotection · Eye
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Notably, the AMPK-activator AICAR mitigates GPR75-induced mitochondrial dysfunction, pyroptosis, and apoptosis.
    1 context sentence
    Summary · context
    To investigate the function of GPR75, we knockdown the receptor in streptozotocin (STZ) mice and high glucose (HG)-treated primary RGCs.

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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