Glycosphingolipids (GSLs) have been implicated as potential atherogenic lipids. Studies in
apolipoprotein E-null (apoE−/−) mice indicate that exacerbated tissue GSL accumulation
resulting from α-galactosidase deficiency promotes atherosclerosis, whereas the serine
palmitoyl transferase inhibitor myriocin (which reduces plasma and tissue levels of several
sphingolipids, including sphingomyelin, ceramide, sphingosine-1-phosphate, and GSLs)
inhibits atherosclerosis. It is not clear whether GSL synthesis inhibition per se has an impact …