The heart switches its main metabolic substrate from glucose to fatty acids shortly after birth, which is one of reasons for the loss of heart regeneration capability in adult mammals. On the contrary, metabolic shifts from oxidative phosphorylation to glucose metabolism promote cardiomyocyte (CM) proliferation after heart injury. However, how glucose transportation in CMs is regulated during heart regeneration is still not fully understood. In this report, we found that the expression of Glut1 (slc2a1) was upregulated around the injury site of zebrafish heart, accompanied by an increase in glucose uptake at the injury area. Knockout ofslc2a1aimpaired zebrafish heart regeneration. Our previous study has demonstrated that the expression ofΔ113p53is activated after heart injury andΔ113p53+CMs undergo proliferation to contribute to zebrafish heart regeneration. Next, we used theΔ113p53promoter to generate theTg(Δ113p53:cmyc)zebrafish transgenic line. Conditional overexpression ofcmycnot only significantly promoted zebrafish CM proliferation and heart regeneration but also significantly enhancedglut1expression at the injury site. Inhibiting Glut1 diminished the increase in CM proliferation inTg(Δ113p53:cmyc)injured hearts of zebrafish. Therefore, our results suggest that the activation ofcmycpromotes heart regeneration through upregulating the expression ofglut1to speed up glucose transportation.