IL1B and hematocrit: These M1 macrophages release a variety of pro‐inflammatory cytokines, such as tumor necrosis factor‐α (TNF‐α) and interleukin‐1β (IL‐1β), which amplify the inflammatory response.[15] Emerging evidence has validated the therapeutic promise of targeted modulation of M1 macrophage polarization in alleviating IR injury during HT.[16] Therefore, elucidating the molecular mechanisms by which M1 macrophages involved in myocardial IR injury could provide critical insights for developing clinical therapies to enhance graft survival in HT.