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RETRACTED: Bartlett et al. Uremic Toxins Activates Na/K-ATPase Oxidant Amplification Loop Causing Phenotypic Changes in Adipocytes in In Vitro Models. <i>Int. J. Mol. Sci.</i> 2018, <i>19</i>, 2685.

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Related Experiment Video

Updated: Sep 9, 2025

Measuring the Rate of Lipolysis in Ex Vivo Murine Adipose Tissue and Primary Preadipocytes Differentiated In Vitro
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Na/K-ATPase Signaling in Adipocytes Promotes Atherosclerosis.

Bruno S Goncalves, Yaxin Wang, Sneha S Pillai

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    Targeting adipocyte Na/K-ATPase (NKA) signaling with Adipo-NaKtide significantly reduced atherosclerosis in mice. This approach also improved metabolic health and lowered inflammation, highlighting NKA as a therapeutic target for cardiometabolic disease.

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    Area of Science:

    • Cardiovascular Research
    • Metabolic Disease
    • Cell Signaling

    Background:

    • Adipocyte dysfunction, oxidative stress, and inflammation are linked to metabolic disturbances and atherosclerosis.
    • Na/K-ATPase (NKA) α1 signaling activates Src kinases, promoting oxidative stress and inflammation.
    • NaKtide, an NKA inhibitor, reduces systemic oxidative stress and inflammation in vivo.

    Purpose of the Study:

    • To investigate the role of adipocyte-specific NKA signaling in atherosclerosis.
    • To evaluate the therapeutic potential of targeting adipocyte NKA in a mouse model of atherosclerosis.

    Main Methods:

    • Adipocyte-specific NKA inhibition using Adipo-NaKtide delivered via lentiviral vector in Apoe-/- mice.
    • Induction of atherosclerosis with a Western Diet for 12 weeks.
    • Assessment of atherosclerotic plaque burden, inflammatory markers, and oxidative stress in adipose tissue and plasma.

    Main Results:

    • Adipo-NaKtide significantly reduced atherosclerotic plaque area in the aortic arch and sinus.
    • Decreased macrophage and smooth muscle cell content within atherosclerotic lesions.
    • Reduced adipose tissue inflammation, oxidative stress, improved glucose tolerance, and lowered systemic inflammation.

    Conclusions:

    • Adipocyte NKA signaling plays a critical role in atherosclerosis development.
    • Adipose tissue influences atherogenesis via endocrine and/or paracrine mechanisms.
    • Targeting NKA represents a potential therapeutic strategy for cardiometabolic diseases.