Reverse cholesterol transport and hepatic osteodystrophy

Cell Metab. 2022 Mar 1;34(3):347-349. doi: 10.1016/j.cmet.2022.02.007.

Abstract

In this issue of Cell Metabolism, Lu et al. show that chronic liver disease increases the expression and activity of PP2Ac, a phosphatase that downregulates the excretion of lecithin-cholesterol aceyltransferase (LCAT). LCAT, a liver-derived enzyme, protects bone and prevents bone loss, and its lowered levels in progressive liver injury cause hepatic osteodystrophy (HOD) and worsen liver fibrosis. These discoveries open the possibility that recombinant LCAT may be a treatment for both HOD and liver fibrosis.

Publication types

  • Research Support, N.I.H., Extramural
  • Comment

MeSH terms

  • Cholesterol* / metabolism
  • Disease Progression
  • Humans
  • Liver Cirrhosis
  • Phosphatidylcholine-Sterol O-Acyltransferase* / biosynthesis

Substances

  • Cholesterol
  • Phosphatidylcholine-Sterol O-Acyltransferase