{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,26]],"date-time":"2026-09-26T20:54:17Z","timestamp":1790456057014,"version":"4.1.0"},"reference-count":71,"publisher":"Oxford University Press (OUP)","issue":"16","license":[{"start":{"date-parts":[[2024,9,19]],"date-time":"2024-09-19T00:00:00Z","timestamp":1726704000000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/academic.oup.com\/pages\/standard-publication-reuse-rights"}],"funder":[{"DOI":"10.13039\/501100001809","name":"National Natural Science Foundation of China","doi-asserted-by":"publisher","award":["82070436"],"award-info":[{"award-number":["82070436"]}],"id":[{"id":"10.13039\/501100001809","id-type":"DOI","asserted-by":"publisher"}]},{"name":"Excellent Doctoral Program of Zhongnan Hospital of Wuhan University","award":["ZNYB202200"],"award-info":[{"award-number":["ZNYB202200"]}]},{"name":"Youth Interdisciplinary Special Fund of Zhongnan Hospital of Wuhan University","award":["ZNQNJC2023001"],"award-info":[{"award-number":["ZNQNJC2023001"]}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2024,12,14]]},"abstract":"<jats:title>Abstract<\/jats:title>\n               <jats:sec>\n                  <jats:title>Aims<\/jats:title>\n                  <jats:p>Interleukin (IL)-12p40 is a common subunit of the bioactive cytokines IL-12 and IL-23, and it also has its own intrinsic functional activity. However, its role in doxorubicin-induced chronic cardiomyopathy (DICCM) as well as the underlying mechanisms are still unknown.<\/jats:p>\n               <\/jats:sec>\n               <jats:sec>\n                  <jats:title>Methods and results<\/jats:title>\n                  <jats:p>In this study, we used IL-12p40-knockout mice, IL-23p19-knockout mice, Rag1-knockout mice, a ferroptosis inhibitor, recombinant IL-12 (rIL-12), rIL-23, rIL-12p40, rIL-12p80, and anti-IL17A to investigate the effects of IL-12p40 on DICCM and elucidate the underlying mechanisms. We found that myocardial ferroptosis were increased in DICCM and that the inhibition of ferroptosis protected against DICCM. The expression of IL-12p40 was upregulated, and IL-12p40 was predominantly expressed by CD4+ T cells in the hearts of mice with DICCM. IL-12p40 knockout attenuated cardiac dysfunction, fibrosis and ferroptosis in DICCM, and similar results were observed in the context of CD4+ T cell IL-12p40 deficiency in Rag1\u2212\/\u2212 mice. Treatment with rIL-23, but not rIL-12, rIL-12p40 monomer or rIL-12p80, abolished the protective effects of IL-12p40 knockout. Moreover, rIL-23 treatment and IL-23p19 knockout exacerbated and ameliorated DICCM, respectively. IL-12p40 knockout might protect against DICCM by inhibiting Th17 differentiation and IL-17A production but not Th1, Th2 and Treg differentiation. Neutralizing IL-17A with an antibody also attenuated cardiac dysfunction, fibrosis, and ferroptosis. The IL-12p40\/Th17\/IL-17A axis might promote cardiomyocyte ferroptosis by activating TNF receptor-associated factor 6 (TRAF6)\/mitogen-activated protein kinase (MAPK)\/P53 signalling in DICCM.<\/jats:p>\n               <\/jats:sec>\n               <jats:sec>\n                  <jats:title>Conclusion<\/jats:title>\n                  <jats:p>Interleukin-12p40 deficiency protects against DICCM by inhibiting Th17 differentiation and the production of IL-17A, which plays critical roles in cardiomyocyte ferroptosis in DICCM via activating TRAF6\/MAPK\/P53 signalling. Our study may provide novel insights for the identification of therapeutic targets for treating DICCM in the clinic.<\/jats:p>\n               <\/jats:sec>","DOI":"10.1093\/cvr\/cvae208","type":"journal-article","created":{"date-parts":[[2024,9,19]],"date-time":"2024-09-19T18:15:17Z","timestamp":1726769717000},"page":"2117-2133","source":"Crossref","is-referenced-by-count":23,"title":["Interleukin-12p40 deficiency attenuates myocardial ferroptosis in doxorubicin-induced chronic cardiomyopathy by inhibiting Th17 differentiation and interleukin-17A production"],"prefix":"10.1093","volume":"120","author":[{"given":"Jishou","family":"Zhang","sequence":"first","affiliation":[{"name":"Department of Cardiology, Renmin Hospital of Wuhan University , 238 Jiefang Road, Wuhan 430060 ,","place":["China"]},{"name":"Department of Cardiology, The First Affiliated Hospital, Zhejiang University School of Medicine , Hangzhou ,","place":["China"]},{"name":"Cardiovascular Research Institute, Wuhan 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