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Scavenging of reactive dicarbonyls with 2-hydroxybenzylamine reduces
atherosclerosis in hypercholesterolemic Ldlr-/- mice.
Authors Tao H, Huang J, Yancey PG, Yermalitsky V, Blakemore JL, Zhang Y, Ding L,
Zagol-Ikapitte I, Ye F, Amarnath V, Boutaud O, Oates JA, Roberts LJ, Davies SS,
Linton MF
Submitted By Submitted Externally on 9/28/2020
Status Published
Journal Nature communications
Year 2020
Date Published 8/1/2020
Volume : Pages 11 : 4084
PubMed Reference 32796843
Abstract Lipid peroxidation generates reactive dicarbonyls including isolevuglandins
(IsoLGs) and malondialdehyde (MDA) that covalently modify proteins. Humans with
familial hypercholesterolemia (FH) have increased lipoprotein dicarbonyl adducts
and dysfunctional HDL. We investigate the impact of the dicarbonyl scavenger,
2-hydroxybenzylamine (2-HOBA) on HDL function and atherosclerosis in Ldlr-/-
mice, a model of FH. Compared to hypercholesterolemic Ldlr-/- mice treated with
vehicle or 4-HOBA, a nonreactive analogue, 2-HOBA decreases atherosclerosis by
60% in en face aortas, without changing plasma cholesterol. Ldlr-/- mice treated
with 2-HOBA have reduced MDA-LDL and MDA-HDL levels, and their HDL display
increased capacity to reduce macrophage cholesterol. Importantly, 2-HOBA reduces
the MDA- and IsoLG-lysyl content in atherosclerotic aortas versus 4-HOBA.
Furthermore, 2-HOBA reduces inflammation and plaque apoptotic cells and promotes
efferocytosis and features of stable plaques. Dicarbonyl scavenging with 2-HOBA
has multiple atheroprotective effects in a murine FH model, supporting its
potential as a therapeutic approach for atherosclerotic cardiovascular disease.


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