{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,7,8]],"date-time":"2026-07-08T10:57:20Z","timestamp":1783508240112,"version":"3.55.0"},"reference-count":34,"publisher":"Wiley","issue":"13","license":[{"start":{"date-parts":[[2024,7,4]],"date-time":"2024-07-04T00:00:00Z","timestamp":1720051200000},"content-version":"vor","delay-in-days":3,"URL":"http:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"funder":[{"DOI":"10.13039\/100007834","name":"Natural Science Foundation of Ningbo Municipality","doi-asserted-by":"publisher","award":["2021J266"],"award-info":[{"award-number":["2021J266"]}],"id":[{"id":"10.13039\/100007834","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["J Cellular Molecular Medi"],"published-print":{"date-parts":[[2024,7]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:p>Interleukin\u20105 (IL\u20105) has been reported to be involved in cardiovascular diseases, such as atherosclerosis and cardiac injury. This study aimed to investigate the effects of IL\u20105 on cardiac remodelling. Mice were infused with angiotensin II (Ang II), and the expression and source of cardiac IL\u20105 were analysed. The results showed that cardiac IL\u20105 expression was time\u2010 and dose\u2010dependently decreased after Ang II infusion, and was mainly derived from cardiac macrophages. Additionally, IL\u20105\u2010knockout (IL\u20105\u2212\/\u2212) mice were used to observe the effects of IL\u20105 knockout on Ang II\u2010induced cardiac remodelling. We found knockout of IL\u20105 significantly increased the expression of cardiac hypertrophy markers, elevated myocardial cell cross\u2010sectional areas and worsened cardiac dysfunction in Ang II\u2010infused mice. IL\u20105 deletion also promoted M2 macrophage differentiation and exacerbated cardiac fibrosis. Furthermore, the effects of IL\u20105 deletion on cardiac remodelling was detected after the STAT3 pathway was inhibited by S31\u2010201. The effects of IL\u20105 on cardiac remodelling and M2 macrophage differentiation were reversed by S31\u2010201. Finally, the effects of IL\u20105 on macrophage differentiation and macrophage\u2010related cardiac hypertrophy and fibrosis were analysed in\u00a0vitro. IL\u20105 knockout significantly increased the Ang II\u2010induced mRNA expression of cardiac hypertrophy markers in myocardial cells that were co\u2010cultured with macrophages, and this effect was reversed by S31\u2010201. Similar trends in the mRNA levels of fibrosis markers were observed when cardiac fibroblasts and macrophages were co\u2010cultured. In conclusions, IL\u20105 deficiency promote the differentiation of M2 macrophages by activating the STAT3 pathway, thereby exacerbating cardiac remodelling in Ang II\u2010infused mice. IL\u20105 may be a potential target for the clinical prevention of cardiac remodelling.<\/jats:p>","DOI":"10.1111\/jcmm.18493","type":"journal-article","created":{"date-parts":[[2024,7,4]],"date-time":"2024-07-04T12:24:35Z","timestamp":1720095875000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":4,"title":["Interleukin\u20105 alleviates cardiac remodelling via the <scp>STAT3<\/scp> pathway in angiotensin <scp>II<\/scp>\u2010infused mice"],"prefix":"10.1111","volume":"28","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-6971-0313","authenticated-orcid":false,"given":"Caijie","family":"Shen","sequence":"first","affiliation":[{"name":"Department of Cardiovascular Medicine The First Affiliated Hospital of Ningbo University  Ningbo China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Nan","family":"Wu","sequence":"additional","affiliation":[{"name":"Department of Cardiovascular Medicine The First Affiliated 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