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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Gajanan D. Katkar
Mahitha Sree Anandachar
Courtney Tindle
University of California, San Diego
Human BioMolecular Research Institute
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Katkar et al. (Tue,) studied this question.
www.synapsesocial.com/papers/69a761cec6e9836116a2fe01 — DOI: https://doi.org/10.64898/2026.02.15.705962