M2 macrophage-derived exosomes (M2-exos) promote angiogenesis and improve cardiac function after myocardial infarction (MI). This study demonstrates that M2-exos enhance cardiac function, reduce infarct size, and improve angiogenesis following MI. The proangiogenic effects of M2-exos are mediated by miR-132-3p, which is enriched in M2-exos and targets THBS1. miR-132-3p binds to the 3'UTR of THBS1, down-regulating its expression and promoting angiogenesis. M2-exos deliver miR-132-3p to endothelial cells (ECs), where it enhances EC viability, proliferation, migration, and tube formation. The study highlights the role of M2-exos in cardiac repair and provides new insights into intercellular communication in post-infarction angiogenesis. M2-exos may serve as a potential therapeutic strategy for myocardial ischemia. The findings suggest that M2-exos improve cardiac function by promoting angiogenesis through miR-132-3p-mediated regulation of THBS1. This study provides a novel understanding of the mechanisms underlying M2-exos in cardiac repair and their potential therapeutic applications.M2 macrophage-derived exosomes (M2-exos) promote angiogenesis and improve cardiac function after myocardial infarction (MI). This study demonstrates that M2-exos enhance cardiac function, reduce infarct size, and improve angiogenesis following MI. The proangiogenic effects of M2-exos are mediated by miR-132-3p, which is enriched in M2-exos and targets THBS1. miR-132-3p binds to the 3'UTR of THBS1, down-regulating its expression and promoting angiogenesis. M2-exos deliver miR-132-3p to endothelial cells (ECs), where it enhances EC viability, proliferation, migration, and tube formation. The study highlights the role of M2-exos in cardiac repair and provides new insights into intercellular communication in post-infarction angiogenesis. M2-exos may serve as a potential therapeutic strategy for myocardial ischemia. The findings suggest that M2-exos improve cardiac function by promoting angiogenesis through miR-132-3p-mediated regulation of THBS1. This study provides a novel understanding of the mechanisms underlying M2-exos in cardiac repair and their potential therapeutic applications.