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Liver X receptor agonists decrease ENaC-mediated sodium transport in collecting duct cells

Sunhapas Soodvilai, Zhanjun Jia, Somsak Fongsupa

    American Journal of Physiology. Renal Physiology
    |October 19, 2012
    PubMed

    Insights

    Liver X receptors (LXRs) regulate metabolism. LXR ligands inhibit epithelial sodium channel (ENaC)-mediated sodium transport in kidney collecting duct cells, suggesting LXRs as a therapeutic target for hypertension.

    Area of Science:

    • Nephrology
    • Endocrinology
    • Molecular Biology

    Background:

    • Liver X receptors (LXRs) are key regulators of lipid, fatty acid, and glucose metabolism.
    • The role of LXRs in renal function, particularly in regulating sodium transport, remains largely unexplored.

    Discussion:

    • LXR agonists T0901317, GW3965, and 22R-hydroxycholesterol reduced amiloride-sensitive sodium transport in M1 collecting duct cells.
    • This inhibition was associated with increased transepithelial resistance and decreased ENaC mRNA and membrane expression, independent of Na+/K+-ATPase activity.
    • LXR activation attenuated aldosterone-stimulated sodium transport and inhibited ENaC function in primary collecting duct cells.

    Key Insights:

    • LXR-activating ligands directly modulate ENaC-mediated sodium transport in kidney collecting duct cells.
    • LXR ligands decrease ENaC abundance and function, impacting sodium reabsorption.
    • These findings reveal a novel mechanism by which LXRs influence renal sodium handling.

    Outlook:

    • LXRs represent a potential therapeutic target for managing conditions characterized by ENaC dysregulation, such as hypertension.
    • Further research into LXR-ENaC interactions could uncover new strategies for blood pressure control.
    • Investigating the precise molecular pathways linking LXR activation to ENaC regulation is warranted.

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