{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,17]],"date-time":"2026-10-17T08:33:27Z","timestamp":1792226007159,"version":"4.4.0"},"reference-count":35,"publisher":"Ovid Technologies (Wolters Kluwer Health)","issue":"5","content-domain":{"domain":["www.ahajournals.org"],"crossmark-restriction":true},"short-container-title":["Circulation"],"published-print":{"date-parts":[[2019,1,29]]},"abstract":"<jats:sec>\n            <jats:title>Background:<\/jats:title>\n            <jats:p>Macrophage-associated immune response plays an important role in myocardial ischemia\/reperfusion (IR) injury. Dectin-1, expressed mainly on activated myeloid cells, is crucial for the regulation of immune homeostasis as a pattern recognition receptor. However, its effects and roles during the myocardial IR injury remain unknown.<\/jats:p>\n          <\/jats:sec>\n          <jats:sec>\n            <jats:title>Methods:<\/jats:title>\n            <jats:p>\n              Genetic ablation, antibody blockade, or Dectin-1 activation, along with the adoptive bone marrow transfer chimeric model, was used to determine the functional significance of Dectin-1 in myocardial IR injury. Immune cell filtration and inflammation were examined by flow cytometry, quantitative real-time polymerase chain reaction, and immunohistochemistry. Moreover, Dectin-1\n              <jats:sup>+<\/jats:sup>\n              cells were analyzed by flow cytometry in the blood of patients with ST-segment\u2013elevation myocardial infarction and stable patients with normal coronary artery (control).\n            <\/jats:p>\n          <\/jats:sec>\n          <jats:sec>\n            <jats:title>Results:<\/jats:title>\n            <jats:p>\n              We demonstrated that Dectin-1 expression observed on the bone marrow\u2013derived macrophages is increased in the heart during the early phase after IR injury. Dectin-1 deficiency and antibody-mediated Dectin-1 inhibition led to a considerable improvement in cardiac function, accompanied by a reduction in cardiomyocyte apoptosis, which was associated with a decrease in M1 macrophage polarization and Ly-6C\n              <jats:sup>+<\/jats:sup>\n              monocyte and neutrophil infiltration. Activation of Dectin-1 with its agonist had the opposite effects. Furthermore, Dectin-1 contributed to neutrophil recruitment through the regulation of Cxcl1 and granulocyte colony-stimulating factor expression. In addition, Dectin-1\u2013dependent interleukin-23\/interleukin-1\u03b2 production was shown to be essential for interleukin-17A expression by \u03b3\u03b4T cells, leading to neutrophil recruitment and myocardial IR injury. Furthermore, we demonstrated that circulating Dectin-1\n              <jats:sup>+<\/jats:sup>\n              CD14\n              <jats:sup>++<\/jats:sup>\n              CD16\n              <jats:sup>\u2212<\/jats:sup>\n              and Dectin-1\n              <jats:sup>+<\/jats:sup>\n              CD14\n              <jats:sup>++<\/jats:sup>\n              CD16\n              <jats:sup>+<\/jats:sup>\n              monocyte levels were significantly higher in patients with ST-segment\u2013elevation myocardial infarction than in controls and positively correlated with the severity of cardiac dysfunction.\n            <\/jats:p>\n          <\/jats:sec>\n          <jats:sec>\n            <jats:title>Conclusions:<\/jats:title>\n            <jats:p>Our results reveal a crucial role of Dectin-1 in the process of mouse myocardial IR injury and provide a new, clinically significant therapeutic target.<\/jats:p>\n          <\/jats:sec>","DOI":"10.1161\/circulationaha.118.036044","type":"journal-article","created":{"date-parts":[[2019,1,17]],"date-time":"2019-01-17T13:44:06Z","timestamp":1547732646000},"page":"663-678","update-policy":"https:\/\/doi.org\/10.1161\/crossmarkpolicy","source":"Crossref","is-referenced-by-count":273,"title":["Dectin-1 Contributes to Myocardial Ischemia\/Reperfusion Injury by Regulating Macrophage Polarization and Neutrophil Infiltration"],"prefix":"10.1161","volume":"139","author":[{"given":"Qin","family":"Fan","sequence":"first","affiliation":[{"name":"Departments of Cardiology (Q.F., R.T., H.Z., H.X., L.L., J.H., Q.Z., W.S., R.Z., X.Y.), Shanghai Jiaotong University School of Medicine, PR China."},{"name":"Rui Jin Hospital, and Institute of Cardiovascular Diseases (Q.F., H.Z., H.X., L.L., Q.C., R.Z., X.Y.), Shanghai Jiaotong University School of Medicine, PR China."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Rong","family":"Tao","sequence":"additional","affiliation":[{"name":"Departments of Cardiology (Q.F., R.T., H.Z., H.X., L.L., J.H., Q.Z., W.S., R.Z., X.Y.), Shanghai Jiaotong University School of Medicine, PR China."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Hang","family":"Zhang","sequence":"additional","affiliation":[{"name":"Departments of Cardiology (Q.F., R.T., H.Z., H.X., L.L., J.H., Q.Z., W.S., R.Z., X.Y.), Shanghai Jiaotong University School of Medicine, PR China."},{"name":"Rui Jin Hospital, and Institute of Cardiovascular Diseases (Q.F., H.Z., H.X., L.L., Q.C., R.Z., X.Y.), Shanghai Jiaotong University School of Medicine, PR China."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Hongyang","family":"Xie","sequence":"additional","affiliation":[{"name":"Departments of Cardiology (Q.F., R.T., H.Z., H.X., L.L., J.H., Q.Z., W.S., R.Z., X.Y.), Shanghai Jiaotong University 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