Fatty acid binding protein 3 deficiency limits atherosclerosis development via macrophage foam cell formation inhibition
Highlights: • We firstly indicated that FABP3 was highly expressed in the aorta of HFD-fed ApoE{sup −/-} mice. • Silencing FABP3 attenuated atherosclerosis due to inhibited macrophage foam cell formation. • FABP3 knockdown decreased foamy macrophage formation partly by inhibiting the PPARγ signal pathway. 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{sup −/-} mice with high-fat-diet (HFD) feeding. Knockdown of FABP3 in HFD-fed ApoE{sup −/-} 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.