Key result
Intravenous angptl2 accelerates atherosclerosis ~10-fold in mice and is elevated in CAD patients.
Why the study?
Angiopoietin-like 2 is overexpressed in endothelial cells from CAD patients, but its contribution to atherogenesis was unknown.
Does angptl2 promote inflammation and atherogenesis in preatherosclerotic dyslipidemic mice?
Population
Preatherosclerotic dyslipidemic mice (LDLr(-/-); hApoB100(+/+)) and endothelial cells from CAD patients and healthy volunteers
Comparison
Exogenous angptl2 vs control or wild-type mice
Design
Preclinical experimental study
Follow-up
1 month
Authors
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No immediate clinical implications; extends preclinical evidence for angptl2 in atherogenesis but requires human validation.
Does angptl2 promote inflammation and atherogenesis in preatherosclerotic dyslipidemic mice?
Effect estimate: 10-fold increase
p-value: p=<0.05
Angptl2 promotes endothelial inflammation and leukocyte adhesion, accelerating atherogenesis in dyslipidemic mice, and is significantly elevated in patients with coronary artery disease.
Farhat et al. (2013) studied Atherosclerosis / Coronary artery disease. Angiopoietin-like 2 (angptl2) vs. Wild-type mice / healthy volunteers was evaluated on Atherosclerotic lesion formation (10-fold increase, p=<0.05). Intravenous administration of angptl2 in preatherosclerotic mice accelerated atherosclerotic lesion formation by 10-fold (P<0.05), and circulating levels were 6-fold higher in CAD patients.
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