Fatty acid binding protein 3 deficiency limits atherosclerosis development via macrophage foam cell formation inhibition.
Exp Cell Res
; 407(1): 112768, 2021 10 01.
Article
em En
| MEDLINE
| ID: mdl-34370993
ABSTRACT
Atherosclerosis is the underlying contributing factor of cardiovascular disease, which is a process of inflammation and lipid-rich lesion. Macrophage-derived foam cell is a key hallmark of atherosclerosis and connected with various factors of lipid metabolism. Here, we showed that fatty acid binding protein 3 (FABP3) was upregulated in the aorta of ApoE-/- mice with high-fat-diet (HFD) feeding. Knockdown of FABP3 in HFD-fed ApoE-/- mice notably facilitated cholesterol efflux, inhibited macrophage foam cell formation, and thus prevented atherogenesis. Furthermore, FABP3 silencing decreased the expression of peroxisome proliferator-activated receptor γ (PPARγ). Mechanistic studies had disclosed the involvement of PPARγ signaling in balancing cholesterol uptake and efflux and diminishing foam cell formation. These findings firstly revealed an anti-atherogenic role of FABP3 silencing in preventing foamy macrophage formation partly through PPARγ, which might be a beneficial approach for therapying atherosclerosis.
Palavras-chave
Texto completo:
1
Coleções:
01-internacional
Base de dados:
MEDLINE
Assunto principal:
Colesterol
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Aterosclerose
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Proteína 3 Ligante de Ácido Graxo
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Macrófagos
Limite:
Animals
Idioma:
En
Ano de publicação:
2021
Tipo de documento:
Article