Table 2.

The potential role of SCP-2 in the pathogenesis of atherosclerosis.

SCP-2 expression	Cells/tissues	Mechanisms	Effects	AS	Ref.
Knockout	Global	Intestinal cholesterol absorption↓, hepatic triglyceride/VLDL secretion↓	Hyperlipidemia↓	↓	63
Overexpression	Rat peritoneal macrophages	ACAT1↑	Cholesterol esterification↑	↑	42,66
Overexpression	Rat aorta	ACAT1↑	Cholesterol esterification↑	↑	69
Overexpression	Mouse L-cell fibroblasts	–	Cholesterol uptake↑	↑	43,73
Overexpression	Mouse L-cell fibroblasts	–	Cholesterol efflux↓	↑	74
Knockdown	Primary mouse hepatocytes	–	Cholesterol efflux↑	↓	75
Overexpression	VSMCs	–	Lipid accumulation↑	↑	41
Overexpression	Liver	LDLR, apoE, apoA-I, and apoB↓, Intestinal cholesterol absorption↑	Hyperlipidemia↑	↑	80
Overexpression	Liver	–	Hepatobiliary cholesterol secretion↑	↑	61,81
Overexpression	Liver	PLOOH and ChOOH transfer↑	Lipid peroxidation↑	↑	26
Suppression	Mouse L-cell fibroblasts	ChOOH transfer and uptake↓	Lipid peroxidation↓	↓	110
Overexpression	Rat hepatoma cells	ChOOH transfer↑	Lipid peroxidation↑	↑	111
Overexpression	HEK 293 Cells	AEA and 2-AG uptake/accumulation↑	Endocannabinoid accumulation↑	↑	119,120
Knockout	Global	AEA and 2-AG accumulation↓	Endocannabinoid accumulation↓	↓	121
Overexpression	Vascular endothelial cells	CD1d-restricted type II NKT cells↑	Vascular inflammation↑	↑	126,127
Overexpression	Mouse L-cell fibroblasts	–	fatty acid uptake, oxidation, and esterification↑	↑	11,102

–, Not determined; AS, atherosclerosis.