influx and efflux. Since macrophages do not have the ability to limit the influx of cholesterol, the balance is completely dependent on efflux pathways. VLDLR is expressed by macrophages, and functions in the uptake of native lipoproteins. Uniquely, VLDLR does not respond to cholesterol loading, likely due to its lack of feedback mechanisms. The inability to control its uptake of native lipoproteins makes VLDLR a pro-atherogenic factor. This characteristic is supported by results from a 2005 study, in which reintroduction of VLDLR into VLDLR knockout mice led to greatly increased atherosclerotic lesion development. See also LDL receptor Very low-density lipoprotein References Further reading External links GeneReviews/NCBI/NIH/UW entry on VLDLR-Associated Cerebellar Hypoplasia or Dysequilibrium Syndrome-VLDLR Low-density lipoprotein receptor gene family