SAMHD1 promotes cardiac repair post myocardial infarction by targeting NR4a1 to regulate macrophage metabolic reprogramming

Our study revealed that macrophage-specific SAMHD1 deletion confers post-MI cardioprotection. More importantly, we demonstrated that NR4a1, a downstream target of SAMHD1, mediates the cardioprotective effects of SAMHD1 deficiency post-MI by regulating the remodeling of macrophage energy metabolism to promote the macrophage reparative phenotype.