biostudies-literatureZhang JNational Natural Science Foundation of ChinaExcellent Doctoral Program of Zhongnan Hospital of Wuhan University324https://www.ebi.ac.uk/biostudies/studies/S-EPMC11072237biostudies-literatureUnknown80(11)Immune response plays a crucial role in post-myocardial infarction (MI) myocardial remodeling. Neogenin (Neo1), a multifunctional transmembrane receptor, plays a critical role in the immune response; however, whether Neo1 participates in pathological myocardial remodeling after MI is unclear. Our study found that Neo1 expression changed significantly after MI in vivo and after LPS + IFN-γ stimulation in bone marrow-derived macrophages (BMDMs) in vitro. Neo1 functional deficiency (using a neutralizing antibody) and macrophage-specific Neo1 deficiency (induced by Neo1^flox/flox;Cx3cr1^cre mice) increased infarction size, enhanced cardiac fibrosis and cardiomyocyte apoptosis, and exacerbated left ventricular dysfunction post-MI in mice. Mechanistically, Neo1 deficiency proCellular and molecular life sciences : CMLSMacrophage neogenin deficiency exacerbates myocardial remodeling and inflammation after acute myocardial infarction through JAK1-STAT1 signaling.PMC11072237ZNYB20220018210029282070436Pan WLiu JZhang JWei CYu JYin ZWang MDing WZhao MQin JJXu SYe DWan JXu YYe JfalseMacrophage neogenin deficiency exacerbates myocardial remodeling and inflammation after acute myocardial infarction through JAK1-STAT1 signaling.Immune response plays a crucial role in post-myocardial infarction (MI) myocardial remodeling. Neogenin (Neo1), a multifunctional transmembrane receptor, plays a critical role in the immune response; however, whether Neo1 participates in pathological myocardial remodeling after MI is unclear. Our study found that Neo1 expression changed significantly after MI in vivo and after LPS + IFN-γ stimulation in bone marrow-derived macrophages (BMDMs) in vitro. Neo1 functional deficiency (using a neutralizing antibody) and macrophage-specific Neo1 deficiency (induced by Neo1^flox/flox;Cx3cr1^cre mice) increased infarction size, enhanced cardiac fibrosis and cardiomyocyte apoptosis, and exacerbated left ventricular dysfunction post-MI in mice. Mechanistically, Neo1 deficiency pro2023-01-01T00:00:00Z2023 Oct2026-06-02T02:20:38.743Z2026-04-13T03:12:15.505ZS-EPMC110722373782402210.1007/s00018-023-04974-7