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2016 ; 8
(333
): 333ra50
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Cyclodextrin promotes atherosclerosis regression via macrophage reprogramming
#MMPMID27053774
Zimmer S
; Grebe A
; Bakke SS
; Bode N
; Halvorsen B
; Ulas T
; Skjelland M
; De Nardo D
; Labzin LI
; Kerksiek A
; Hempel C
; Heneka MT
; Hawxhurst V
; Fitzgerald ML
; Trebicka J
; Björkhem I
; Gustafsson JÅ
; Westerterp M
; Tall AR
; Wright SD
; Espevik T
; Schultze JL
; Nickenig G
; Lütjohann D
; Latz E
Sci Transl Med
2016[Apr]; 8
(333
): 333ra50
PMID27053774
show ga
Atherosclerosis is an inflammatory disease linked to elevated blood cholesterol
concentrations. Despite ongoing advances in the prevention and treatment of
atherosclerosis, cardiovascular disease remains the leading cause of death
worldwide. Continuous retention of apolipoprotein B-containing lipoproteins in
the subendothelial space causes a local overabundance of free cholesterol.
Because cholesterol accumulation and deposition of cholesterol crystals (CCs)
trigger a complex inflammatory response, we tested the efficacy of the cyclic
oligosaccharide 2-hydroxypropyl-?-cyclodextrin (CD), a compound that increases
cholesterol solubility in preventing and reversing atherosclerosis. We showed
that CD treatment of murine atherosclerosis reduced atherosclerotic plaque size
and CC load and promoted plaque regression even with a continued cholesterol-rich
diet. Mechanistically, CD increased oxysterol production in both macrophages and
human atherosclerotic plaques and promoted liver X receptor (LXR)-mediated
transcriptional reprogramming to improve cholesterol efflux and exert
anti-inflammatory effects. In vivo, this CD-mediated LXR agonism was required for
the antiatherosclerotic and anti-inflammatory effects of CD as well as for
augmented reverse cholesterol transport. Because CD treatment in humans is safe
and CD beneficially affects key mechanisms of atherogenesis, it may therefore be
used clinically to prevent or treat human atherosclerosis.
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