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The circadian clock component BMAL1 enhances macrophage inflammation by nuclear translocation of peroxisomal β-oxidation enzyme MFP2
The body clock protein BMAL1 increases inflammation in immune cells by moving a fat-processing enzyme into the nucleus
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Abstract
BMAL1 enhances macrophage inflammation by promoting the nuclear activity of the enzyme MFP2.
- BMAL1 drives the accumulation of MFP2 in the nucleus, increasing inflammatory responses.
- Nuclear MFP2 is involved in producing acetyl-CoA and modifying the NF-κB protein, which promotes inflammation.
- Levels of nuclear MFP2 fluctuate daily in the liver, but this pattern is disrupted in mice lacking BMAL1.
- Removing BMAL1 specifically in macrophages reduces liver inflammation and tumor growth linked to chemical exposure.
- These findings indicate a metabolic pathway regulated by BMAL1 that connects circadian rhythms to macrophage-related inflammation.
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