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Corrigendum

    Insights

    Dapagliflozin helps relax blood vessels and reduces the activation of human vascular endothelial cells, potentially preventing atherosclerosis. This study clarifies a minor typographical error in primer sequences that did not affect the results.

    Area of Science:

    • Cardiovascular Research
    • Endocrinology
    • Molecular Biology

    Background:

    • Atherosclerosis is a chronic inflammatory disease driven by endothelial cell activation.
    • Dapagliflozin, a sodium-glucose cotransporter-2 inhibitor, has shown potential cardiovascular benefits.
    • Understanding the molecular mechanisms of dapagliflozin's vascular effects is crucial.

    Purpose of the Study:

    • To investigate the effects of dapagliflozin on human vascular endothelial cell activation.
    • To explore dapagliflozin's role in inducing vasorelaxation.
    • To assess the potential of dapagliflozin in inhibiting atherogenesis.

    Main Methods:

    • Human umbilical vein endothelial cells (HUVECs) were treated with dapagliflozin.
    • Cellular activation markers, including nuclear factor-kappa B (NFκB) signaling, were assessed.
    • Vasorelaxation assays were performed.
    • A typographical error in the NFκB reverse primer sequence was identified and corrected; this correction did not impact experimental validity.

    Main Results:

    • Dapagliflozin treatment attenuated endothelial cell activation.
    • Dapagliflozin induced vasorelaxation in pre-contracted vessels.
    • NFκB activation was modulated by dapagliflozin.

    Conclusions:

    • Dapagliflozin exhibits anti-atherogenic properties by reducing endothelial cell activation and promoting vasorelaxation.
    • These vascular effects represent a potential mechanism for dapagliflozin's cardioprotective actions.
    • The identified primer sequence correction ensures clarity without compromising study findings.

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