Moreover, MMP-28 has garnered attention for its ability to augment the activation of M2 macrophages, thereby exerting a protective effect against cardiac rupture following MI (130).Furthermore, studies focusing on macrophage-specific Lgr4 deletion have unveiled a compelling mechanistic link, wherein ablation of this receptor culminates in a discernible shift in macrophage subtype composition within the infarcted milieu, characterized by a decrease in M1 macrophages juxtaposed with an augmentation in M2 macrophages, ultimately translating into a lowered incidence of cardiac rupture (65). This evidence concerns the gene LGR4 and myocardial infarction.