{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Zhang J"],"funding":["National Natural Science Foundation of China","Excellent Doctoral Program of Zhongnan Hospital of Wuhan University"],"pagination":["324"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC11072237"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["80(11)"],"pubmed_abstract":["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<sup>flox/flox</sup>;Cx3cr1<sup>cre</sup> mice) increased infarction size, enhanced cardiac fibrosis and cardiomyocyte apoptosis, and exacerbated left ventricular dysfunction post-MI in mice. Mechanistically, Neo1 deficiency pro"],"journal":["Cellular and molecular life sciences : CMLS"],"pubmed_title":["Macrophage neogenin deficiency exacerbates myocardial remodeling and inflammation after acute myocardial infarction through JAK1-STAT1 signaling."],"pmcid":["PMC11072237"],"funding_grant_id":["ZNYB2022001","82100292","82070436"],"pubmed_authors":["Pan W","Liu J","Zhang J","Wei C","Yu J","Yin Z","Wang M","Ding W","Zhao M","Qin JJ","Xu S","Ye D","Wan J","Xu Y","Ye J"],"additional_accession":[]},"is_claimable":false,"name":"Macrophage neogenin deficiency exacerbates myocardial remodeling and inflammation after acute myocardial infarction through JAK1-STAT1 signaling.","description":"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<sup>flox/flox</sup>;Cx3cr1<sup>cre</sup> mice) increased infarction size, enhanced cardiac fibrosis and cardiomyocyte apoptosis, and exacerbated left ventricular dysfunction post-MI in mice. Mechanistically, Neo1 deficiency pro","dates":{"release":"2023-01-01T00:00:00Z","publication":"2023 Oct","modification":"2026-06-02T02:20:38.743Z","creation":"2026-04-13T03:12:15.505Z"},"accession":"S-EPMC11072237","cross_references":{"pubmed":["37824022"],"doi":["10.1007/s00018-023-04974-7"]}}