CCND1 expression decreases in monocytes and cardiac macrophages after myocardial infarction (MI), correlating with adverse cardiac remodeling.
Macrophage-specific deletion of CCND1 exacerbates inflammation and worsens cardiac dysfunction following MI.
CCND1 interacts with PDK4, facilitating its ubiquitination via RPL11 and MDM2, suppressing PDK4’s phosphorylation of PDH, thereby enhancing glucose oxidation in macrophages.
Therapeutic targeting of the CCND1-PDK4 axis in macrophages promotes reparative phenotype transition, improving cardiac function post-MI independently of CCND1’s cell cycle role.
