{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,4,24]],"date-time":"2026-04-24T06:44:03Z","timestamp":1777013043418,"version":"3.51.4"},"reference-count":54,"publisher":"Wiley","issue":"4","license":[{"start":{"date-parts":[[2026,4,23]],"date-time":"2026-04-23T00:00:00Z","timestamp":1776902400000},"content-version":"vor","delay-in-days":22,"URL":"http:\/\/creativecommons.org\/licenses\/by\/4.0\/"},{"start":{"date-parts":[[2026,4,1]],"date-time":"2026-04-01T00:00:00Z","timestamp":1775001600000},"content-version":"tdm","delay-in-days":0,"URL":"http:\/\/doi.wiley.com\/10.1002\/tdm_license_1.1"}],"funder":[{"DOI":"10.13039\/501100001809","name":"National Natural Science Foundation of China","doi-asserted-by":"publisher","award":["82400406"],"award-info":[{"award-number":["82400406"]}],"id":[{"id":"10.13039\/501100001809","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100012166","name":"National Key Research and Development Program of China","doi-asserted-by":"publisher","award":["2019YFE0113900"],"award-info":[{"award-number":["2019YFE0113900"]}],"id":[{"id":"10.13039\/501100012166","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Clinical & Translational Med"],"published-print":{"date-parts":[[2026,4]]},"abstract":"Abstract<\/jats:title>\n \n Background<\/jats:title>\n Cardiac macrophages (cMacs) have been implicated in myocardial repair following myocardial infarction (MI), yet their therapeutic potential in ischaemic cardiomyopathy (ICM) remains limited by an incomplete understanding of their molecular regulation. Cluster of Differentiation 163 (CD163) is highly expressed in these macrophages, yet its functional role in regulating post\u2010MI cardiac repair remains unknown.<\/jats:p>\n <\/jats:sec>\n \n Methods<\/jats:title>\n \n A cross\u2010sectional clinical study was conducted to assess the association between circulating soluble CD163 concentration and heart failure due to ICM. To investigate the functional contribution of CD163 in ICM, wild\u2010type (WT) and\n Cd163<\/jats:italic>\n \u2212<\/jats:sup>\n \n \/<\/jats:sup>\n <\/jats:italic>\n \u2212<\/jats:sup>\n mice were subjected to permanent ligation of the left anterior descending coronary artery. Single\u2010cell RNA sequencing was employed to analyse transcriptional changes in cardiac immune cells. Recombinant osteopontin (OPN) and CD163 were administered to assess their therapeutic effect in\n Cd163<\/jats:italic>\n \u2212<\/jats:sup>\n \n \/<\/jats:sup>\n <\/jats:italic>\n \u2212<\/jats:sup>\n mice.\n <\/jats:p>\n <\/jats:sec>\n \n Results<\/jats:title>\n \n Circulating soluble CD163 levels were markedly elevated in patients with ICM\u2010induced heart failure compared with individuals without heart failure (median difference 34.5\u00a0ng\/mL, IQR 13.6\u201354.6\u00a0ng\/mL,\n p<\/jats:italic>\n \u00a0=\u00a0.002) and showed a positive correlation with the extent of systolic dysfunction and left ventricular (LV) dilation.\n Cd163<\/jats:italic>\n \u2212<\/jats:sup>\n \n \/<\/jats:sup>\n <\/jats:italic>\n \u2212<\/jats:sup>\n mice displayed aggravated LV systolic dysfunction, reduced ejection fraction and fractional shortening, impaired myocardial strain and reduced relative wall thickness post\u2010MI. Recombinant CD163 protein could reverse systolic dysfunction and LV dilation in\n Cd163<\/jats:italic>\n \u2212<\/jats:sup>\n \n \/<\/jats:sup>\n <\/jats:italic>\n \u2212<\/jats:sup>\n mice after MI. CD163 was predominantly expressed in CCR2\n \u2212<\/jats:sup>\n resident cMacs, and CD163 deficiency altered transcriptional programmes of macrophages without affecting their polarization status, with enrichment in cytokine signalling and extracellular matrix\u2010related pathways.\n Spp1<\/jats:italic>\n (OPN) expression was significantly downregulated in\n Cd163<\/jats:italic>\n \u2212<\/jats:sup>\n \n \/<\/jats:sup>\n <\/jats:italic>\n \u2212<\/jats:sup>\n hearts under both sham and MI conditions. Administration of recombinant OPN improved systolic function, reduced ventricular dilation, decreased fibrotic scar size and restored the elastin\u2010to\u2010collagen ratio in\n Cd163<\/jats:italic>\n \u2212<\/jats:sup>\n \n \/<\/jats:sup>\n <\/jats:italic>\n \u2212<\/jats:sup>\n mice.\n <\/jats:p>\n <\/jats:sec>\n \n Conclusions<\/jats:title>\n In cMacs, CD163 contributes to post\u2010MI repair by upregulating OPN expression, which in turn helps maintain systolic function.<\/jats:p>\n <\/jats:sec>\n \n Key points<\/jats:title>\n \n \n \n Soluble CD163 is elevated in ICM and correlates with LV dysfunction.<\/jats:p>\n <\/jats:list-item>\n \n \n Cd163<\/jats:italic>\n \u2212<\/jats:sup>\n \n \/<\/jats:sup>\n <\/jats:italic>\n \u2212<\/jats:sup>\n mice show worsened post\u2010MI systolic dysfunction and dilation.\n <\/jats:p>\n <\/jats:list-item>\n \n \n Recombinant CD163 reverses dysfunction in\n Cd163<\/jats:italic>\n \u2212<\/jats:sup>\n \n \/<\/jats:sup>\n <\/jats:italic>\n \u2212<\/jats:sup>\n mice.\n <\/jats:p>\n <\/jats:list-item>\n \n \n OPN restores function and improves LV structure in\n Cd163<\/jats:italic>\n \u2212<\/jats:sup>\n \n \/<\/jats:sup>\n <\/jats:italic>\n \u2212<\/jats:sup>\n mice.\n <\/jats:p>\n <\/jats:list-item>\n <\/jats:list>\n <\/jats:p>\n <\/jats:sec>","DOI":"10.1002\/ctm2.70662","type":"journal-article","created":{"date-parts":[[2026,4,24]],"date-time":"2026-04-24T04:47:49Z","timestamp":1777006069000},"source":"Crossref","is-referenced-by-count":0,"title":["Macrophage Cluster of Differentiation 163 promotes post\u2010infarction cardiac repair and preserves left ventricular function via osteopontin"],"prefix":"10.1002","volume":"16","author":[{"given":"Jingyu","family":"Chen","sequence":"first","affiliation":[{"name":"Xiamen Cardiovascular Hospital School of Medicine Xiamen University Xiamen 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