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However, the effects of IL\u20107 on macrophages infiltration and polarization in myocardial I\/R injury are currently unclear. This study aimed to evaluate the effects of the IL\u20107 expression on myocardial I\/R injury and their relationship with macrophages. The data showed that IL\u20107 expression in mouse heart tissue increases following I\/R injury and that IL\u20107 knockout or anti\u2010IL\u20107 antibody treatment significantly improve I\/R injury, including reduction in myocardial infarction area, a serum troponin T level decreases and an improvement in cardiac function. On the other hand, recombinant IL\u20107 (rIL\u20107) supplementation induces opposite effects and the anti\u2010IL\u20107 antibody significantly reduces the cardiomyocyte apoptosis and macrophage infiltration. rIL\u20107 cannot directly cause apoptosis, but it can induce cardiomyocyte apoptosis through macrophages, in addition to increase the macrophages migration in vitro. Anti\u2010IL\u20107 antibody affects the cytokine production in T helper (Th) 1 and Th2 cells and also promotes the macrophages differentiation to M2 macrophages. However, anti\u2010IL\u20107 antibody does not reduce the M1 macrophage number, and it only increases the ratio of M2\/M1 macrophages in mice heart tissues after I\/R injury. Taking together, these data reveal that IL\u20107 plays an intensifying role in myocardial I\/R injury by promoting cardiomyocyte apoptosis through the regulation of macrophage infiltration and polarization.<\/jats:p>","DOI":"10.1111\/jcmm.16335","type":"journal-article","created":{"date-parts":[[2021,9,28]],"date-time":"2021-09-28T03:54:57Z","timestamp":1632801297000},"page":"9939-9952","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":26,"title":["Interleukin\u20107 aggravates myocardial ischaemia\/reperfusion injury by regulating macrophage infiltration and polarization"],"prefix":"10.1111","volume":"25","author":[{"given":"Mengwen","family":"Yan","sequence":"first","affiliation":[{"name":"Department of Cardiology China\u2010Japan Friendship Hospital Beijing China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yaliu","family":"Yang","sequence":"additional","affiliation":[{"name":"Department of Cardiology China\u2010Japan Friendship Hospital Beijing China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ying","family":"Zhou","sequence":"additional","affiliation":[{"name":"Department of Cardiology China\u2010Japan Friendship Hospital Beijing China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Changan","family":"Yu","sequence":"additional","affiliation":[{"name":"Central Laboratory of Cardiovascular Disease China\u2010Japan Friendship Hospital Beijing China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Rui","family":"Li","sequence":"additional","affiliation":[{"name":"Department of Health Care China\u2010Japan Freindship Hospital Ministry of Health Beijing China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-3298-7001","authenticated-orcid":false,"given":"Wei","family":"Gong","sequence":"additional","affiliation":[{"name":"Emergency and Critical Care Center Beijing Anzhen Hospital Capital Medical University Beijing China"},{"name":"Beijing Institute of Heart, Lung, and Blood Vessel Diseases Beijing China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jingang","family":"Zheng","sequence":"additional","affiliation":[{"name":"Department of Cardiology China\u2010Japan Friendship Hospital Beijing China"},{"name":"Department of Cardiology China\u2010Japan Friendship School of Clinical Medicine Peking Union Medical College Chinese Academy of Medical Sciences Beijing China"},{"name":"Department of Cardiology Peking University China\u2010Japan Friendship School of Clinical Medicine Beijing China"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"311","published-online":{"date-parts":[[2021,9,28]]},"reference":[{"key":"e_1_2_9_2_1","doi-asserted-by":"publisher","DOI":"10.1161\/CIR.0b013e31823a5596"},{"key":"e_1_2_9_3_1","doi-asserted-by":"publisher","DOI":"10.1016\/S0003-4975(01)02400-6"},{"key":"e_1_2_9_4_1","doi-asserted-by":"publisher","DOI":"10.1016\/j.hoc.2006.11.010"},{"issue":"1","key":"e_1_2_9_5_1","first-page":"0","article-title":"IL\u20107 and IL\u201015: therapeutic cytokines for immunodeficiency","volume":"26","author":"Alpdogan n, Brink MRMvd","journal-title":"Trends Immunol"},{"key":"e_1_2_9_6_1","doi-asserted-by":"publisher","DOI":"10.1007\/s00262-011-1159-3"},{"key":"e_1_2_9_7_1","doi-asserted-by":"publisher","DOI":"10.1002\/eji.200425532"},{"key":"e_1_2_9_8_1","doi-asserted-by":"publisher","DOI":"10.2174\/138161212800165979"},{"key":"e_1_2_9_9_1","first-page":"728","article-title":"Macrophages are the primary effector cells in IL\u20107\u2010induced arthritis","volume":"1","author":"Kim S\u2010J","year":"2019","journal-title":"Cell Mol Immunol"},{"key":"e_1_2_9_10_1","doi-asserted-by":"publisher","DOI":"10.1111\/jcmm.13610"},{"key":"e_1_2_9_11_1","doi-asserted-by":"publisher","DOI":"10.1016\/j.neuroscience.2017.10.022"},{"issue":"5","key":"e_1_2_9_12_1","first-page":"1","article-title":"Inflammation perturbs the IL\u20107 axis, promoting senescence and exhaustion that broadly characterize immune failure in treated HIV infection","volume":"71","author":"Shive CL","year":"2015","journal-title":"J Acqui Immune Defic Syndr"},{"key":"e_1_2_9_13_1","doi-asserted-by":"publisher","DOI":"10.1038\/ni.1689"},{"key":"e_1_2_9_14_1","doi-asserted-by":"publisher","DOI":"10.2174\/1568010054022024"},{"key":"e_1_2_9_15_1","doi-asserted-by":"publisher","DOI":"10.1016\/j.lfs.2016.02.039"},{"key":"e_1_2_9_16_1","unstructured":"ChengY RongJ.Prostaglandin 15\u2010keto PGF2\u03b1 skews macrophage M1\/M2 polarization against myocardial ischemia reperfusion injury via covalent modification of glycolytic enzyme PKM2. 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