March 3, 2026Open Access

A Druggable G Protein Checkpoint in Cholesterol Efflux

Puntos clave

GIV loss promotes macrophage cholesterol efflux, leading to reduced plaque burden and improved lipid profiles.
Inhibition of the GIV●Gαi checkpoint has shown effective cholesterol regulation in studies of lipid overload conditions.
Analysis highlights the G protein's role in mediating ABCA1 activity through both transcriptional and post-translational mechanisms.
These findings suggest new avenues for treatment strategies in immunometabolic diseases and highlight cholesterol management.

Resumen

Statins slow but rarely reverse plaque burden, leaving residual risk driven by LAM dysfunctionGIV (CCDC88A) non-canonically modulates Gαi to suppress macrophage cholesterol effluxGIV loss or inhibition restores ABCA1 activity via transcriptional and post-translational controlBlocking the GIV●Gαi checkpoint defats LAMs, regresses plaques, and relieves systemic lipid overloadIdentifies a druggable node that redefines RCT restoration as a therapeutic paradigm in immunometabolic disease.

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Cite This Study

Katkar et al. (Tue,) studied this question.

synapsesocial.com/papers/69a761cec6e9836116a2fe01 https://doi.org/https://doi.org/10.64898/2026.02.15.705962

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