Fucoxanthin prevents septic cardiomyopathy by targeting BRD2 in M1-polarized macrophages

that provoked inflammation in cardiomyocytes. Further, bromodomain-containing protein 2 (BRD2) was predicted as a molecular target of FX. Moreover, FX decreased BRD2 protein in both mouse hearts and macrophages in the presence of LPS. BRD2 overexpression abolished FX's macrophage-silencing effect. Notably, FX decreased BRD2 levels and inhibited inflammation in peripheral monocyte-derived macrophages from patients with SCM. The present study offers FX and BRD2 as a novel approach and molecular target for SCM intervention.