The circadian clock component BMAL1 enhances macrophage inflammation by nuclear translocation of peroxisomal β-oxidation enzyme MFP2

Using H3K27ac ChIP‑seq, we analyzed genome‑wide histone H3 lysine 27 acetylation (H3K27ac) in wild‑type, Bmal1‑deficient, and Mfp2‑deficient RAW264.7 cells, a mouse macrophage‑like cell line. Comparative analyses revealed substantial overlap in H3K27ac regions reduced upon loss of BMAL1 or MFP2, suggesting a coordinated BMAL1–MFP2 axis in the regulation of inflammation‑associated chromatin states.