Cardiovascular diseases, such as myocardial infarction (MI), are a leading cause of death worldwide. Acute MI (AMI) inflicts massive injury to the coronary microcirculation, causing large-scale cardiomyocyte death due to ischemia and hypoxia. Inflammatory cells such as monocytes and macrophages migrate to the damaged area to clear away dead cells post-MI. Macrophages are pleiotropic cells of the innate immune system, which play an essential role in the initial inflammatory response that occurs following MI, inducing subsequent damage and facilitating recovery. Besides their recognized role within the immune response, macrophages participate in crosstalk with other cells (including cardiomyocytes, fibroblasts, immune cells, and vascular endothelial cells) to coordinate post-MI processes within cardiac tissue. Macrophage-secreted exosomes have recently attracted increasing attention, which has led to a more elaborate understanding of macrophage function. Currently, the functional roles of macrophages in the microenvironment of the infarcted heart, particularly with regard to their interaction with surrounding cells, remain unclear. Understanding the specific mechanisms that mediate this crosstalk is essential in treating MI. In this review, we discuss the origin of macrophages, changes in their distribution post-MI, phenotypic and functional plasticity, as well as the specific signaling pathways involved, with a focus on the crosstalk with other cells in the heart. Thus, we provide a new perspective on the treatment of MI. Further in-depth research is required to elucidate the mechanisms underlying crosstalk between macrophages and other cells within cardiac tissue for the identification of potential therapeutic targets.Video AbstractSupplementary InformationThe online version contains supplementary material available at 10.1186/s12964-023-01105-4.