ACAT inhibition reduces the progression of preexisting, advanced atherosclerotic
mouse lesions without plaque or systemic toxicity.
Authors Rong JX, Blachford C, Feig JE, Bander I, Mayne J, Kusunoki J, Miller C, Davis M,
Wilson M, Dehn S, Thorp E, Tabas I, Taubman MB, Rudel LL, Fisher EA
Submitted By Edward Fisher on 3/4/2015
Status Published
Journal Arteriosclerosis, thrombosis, and vascular biology
Year 2013
Date Published 1/1/2013
Volume : Pages 33 : 4 - 12
PubMed Reference 23139293
Abstract Acyl-CoA:cholesterol acyltransferase (ACAT) converts cholesterol to cholesteryl
esters in plaque foam cells. Complete deficiency of macrophage ACAT has been
shown to increase atherosclerosis in hypercholesterolemic mice because of
cytotoxicity from free cholesterol accumulation, whereas we previously showed
that partial ACAT inhibition by Fujirebio compound F1394 decreased early
atherosclerosis development. In this report, we tested F1394 effects on
preestablished, advanced lesions of apolipoprotein-E-deficient mice.

Investigators with authorship
Edward FisherNew York University School of Medicine