January 2016
Volume 57Issue 1p1-156
Open Access
COVER: In this issue of the Journal of Lipid Research, the LMK model, an in silico model of lipoprotein metabolism and kinetics shown schematically
in the diagram, was utilized to analyze how HDL modulating interventions affect the
rate of reverse cholesterol transport (RCT). The LMK model represents the RCT pathway
from lipid-poor ApoA-I to mature HDL and the transfers of HDL-cholesterol to and from
other lipoproteins. The set of interventions that were analyzed are numbered in the
diagram: (1) upregulation of ApoA-I synthesis; (2) infusion of rHDL; (3) infusion
of delipidated HDL; (4) upregulation of ABCA1; (5) inhibition of CETP. A commentary
by Robert Phair (see p. 1 of this issue) discusses this work in the context of the decades-long tradition of
collaboration between experimentalists and mathematical modelers. (See Gadkar et al., p. 46.)...Show more
COVER: In this issue of the Journal of Lipid Research, the LMK model, an in silico model of lipoprotein metabolism and kinetics shown schematically
in the diagram, was utilized to analyze how HDL modulating interventions affect the
rate of reverse cholesterol transport (RCT). The LMK model represents the RCT pathway
from lipid-poor ApoA-I to mature HDL and the transfers of HDL-cholesterol to and from
other lipoproteins. The set of interventions that were analyzed are numbered in the
diagram: (1) upregulation of ApoA-I synthesis; (2) infusion of rHDL; (3) infusion
of delipidated HDL; (4) upregulation of ABCA1; (5) inhibition of CETP. A commentary
by Robert Phair (see p. 1 of this issue) discusses this work in the context of the decades-long tradition of
collaboration between experimentalists and mathematical modelers. (See Gadkar et al., p. 46.)
