Figure 2.

Schematic representation of cardiac macrophages initiating cardiomyocyte proliferation and repair. During the inflammatory response to myocardial injury, oncostatin M (OSM) secreted by cardiac infiltrating macrophages binds to the type II receptor Gp130 and stimulates Src-enhanced YAP phosphorylation to promote cardiomyocyte proliferation and myocardial repair. Meanwhile, the cardiac resident macrophage subpopulation MP1 (CX₃CR1⁺CCR2⁻Ly6C⁻MHCII⁻) directly triggered cardiomyocyte proliferation via the Jagged-1-Notch1 axis, significantly ameliorating cardiac injury after myocardial infarction. The glycolytic metabolite lactate dehydrogenase A (LDHA) creates a beneficial cardiac regenerative microenvironment through the polarization of M2 macrophages. The iron-regulating hormone hepcidin and interleukin (IL)-4/6 enhance cellular plasticity and adaptation of the extracellular matrix microenvironment, facilitating cardiac regeneration and repair.