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Updated: Oct 2, 2025

Digital Planimetry for Assessing Wound Closure Kinetics in a Mouse Model
07:56

Digital Planimetry for Assessing Wound Closure Kinetics in a Mouse Model

Published on: January 10, 2025

786

Retraction

    Journal of Cellular Physiology
    |February 23, 2022
    PubMed

    Insights

    This study on kidney stones is retracted due to unintentional errors in the research process. The findings regarding gastrin-releasing peptide receptor gene silencing and its effects on epithelial-mesenchymal transition are now considered invalid.

    Area of Science:

    • Cell Biology
    • Molecular Biology
    • Nephrology

    Context:

    • Kidney stones, specifically calcium oxalate crystal formation, pose a significant health challenge.
    • The epithelial-mesenchymal transition (EMT) is implicated in the pathogenesis of kidney stone development.
    • Signaling pathways, such as PI3K/Akt, are crucial in cellular processes relevant to kidney stone formation.

    Purpose:

    • To investigate the role of gastrin-releasing peptide receptor (GRPR) gene silencing in inhibiting EMT and calcium oxalate crystal formation in renal tubular epithelial cells.
    • To elucidate the involvement of the PI3K/Akt signaling pathway in the observed effects.

    Summary:

    • The study aimed to explore how silencing the GRPR gene impacts EMT and calcium oxalate crystal formation in mouse kidney stone models.
    • The research focused on the PI3K/Akt signaling pathway as a potential mediator of these effects.
    • However, the article has been retracted due to unintentional errors and unverifiable experimental results, rendering the conclusions invalid.

    Impact:

    • The retraction indicates that the initially reported findings on GRPR gene silencing and its influence on kidney stone development via the PI3K/Akt pathway are not scientifically supported.
    • This highlights the importance of rigorous verification in scientific research and the potential impact of errors on established conclusions.
    • Further research is needed to clarify the actual role of GRPR and the PI3K/Akt pathway in kidney stone pathogenesis.

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