Complete and Partial LCAT Deficiency are Differentially Associated with Atherosclerosis

Lecitina:colesterolo aciltransferasi: un possibile target terapeutico per ridurre l'aterosclerosi? (Circulation 2018 May 10)

23 May May 2018 one year ago
  • Baldassarre D, Amato M, Barbieri S, Veglia F

Lecithin:cholesterol acyltransferase (LCAT) is the sole enzyme that esterifies cholesterol in plasma. Its role in the supposed protection from atherogenesis remains unclear since mutations in LCAT causing Fish-Eye Disease (FED) or Familial LCAT Deficiency (FLD) have been reported to be associated with more or instead less carotid atherosclerosis, respectively. This discrepancy may be associated with the loss of cholesterol esterification on only apolipoprotein (apo) A-I (FED) or on both apoA-I and apoB-containing lipoproteins (FLD), an aspect that has thus far not been investigated.

In this head-to-head comparison, these two disorder of lipoprotein metabolism were shown to be associated with decreased and increased atherosclerosis, respectively. The Authors propose that this discrepancy is related to the capacity of LCAT to generate cholesterol esters on apoB-containing lipoproteins. While this capacity is lost in FLD, it is unaffected in FED. These results are important when considering LCAT as a target to decrease atherosclerosis.

1. Oldoni F, Baldassarre D, Castelnuovo S, Ossoli A, Amato M, van Capelleveen J, Hovingh GK, de Groot E, Bochem A, Simonelli S, Barbieri S, Veglia F, Franceschini G, Kuivenhoven JA, Holleboom AG, Calabresi L. Complete and Partial LCAT Deficiency are Differentially Associated with Atherosclerosis. Circulation 2018 May 10. pii: CIRCULATIONAHA.118.034706. doi: 10.1161/CIRCULATIONAHA.118.034706. [Epub ahead of print] → Download PDF