1. Fatty acid binding protein 3 deficiency limits atherosclerosis development via macrophage foam cell formation inhibition.
- Author
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Tan L, Lu J, Liu L, and Li L
- Subjects
- Animals, Fatty Acid Binding Protein 3 metabolism, Lipid Metabolism physiology, Macrophages pathology, Macrophages, Peritoneal metabolism, PPAR gamma metabolism, Atherosclerosis metabolism, Atherosclerosis pathology, Cholesterol metabolism, Fatty Acid Binding Protein 3 deficiency, Macrophages metabolism
- 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., (Copyright © 2021 Elsevier Inc. All rights reserved.)- Published
- 2021
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