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Here, we examined the signalling and phenotypic effects of inhibiting IL11 signalling using neutralizing antibodies against IL11 or its cognate receptor (IL11RA) in a mouse model of acute and severe pressure overload. C57BL\/6J mice underwent ascending aortic constriction (AAC) surgery and were randomized to anti\u2010IL11, anti\u2010IL11RA, or isotype control antibodies (20\u00a0mg\/kg, bi\u2010weekly for 2\u00a0weeks). AAC surgery induced the expression of IL11, IL11RA and extracellular matrix (ECM) genes that was associated with cardiac hypertrophy and aortic remodelling. Inhibition of IL11 signalling reduced AAC\u2010induced cardiac fibrosis and ECM gene expression as well as ERK1\/2 phosphorylation but had no effect on cardiac hypertrophy. STAT3 was phosphorylated in the hearts of AAC\u2010treated mice but this was unrelated to IL11 activity, which we confirmed in mouse cardiac fibroblasts in vitro. These data highlight that blocking IL11 signalling reduces cardiac fibrosis due to severe pressure overload and suggests ERK, but not STAT3, activity as the relevant underlying signalling pathway.<\/jats:p>","DOI":"10.1111\/1440-1681.13458","type":"journal-article","created":{"date-parts":[[2021,1,19]],"date-time":"2021-01-19T02:11:30Z","timestamp":1611022290000},"page":"605-613","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":17,"title":["Antibody\u2010mediated neutralization of IL11 signalling reduces ERK activation and cardiac fibrosis in a mouse model of severe pressure overload"],"prefix":"10.1111","volume":"48","author":[{"ORCID":"https:\/\/orcid.org\/0000-0003-0311-943X","authenticated-orcid":false,"given":"Wei\u2010Wen","family":"Lim","sequence":"first","affiliation":[{"name":"National Heart Research Institute Singapore National Heart Centre Singapore Singapore Singapore"},{"name":"Cardiovascular and Metabolic Disorders Program Duke\u2010National University of Singapore Medical School Singapore Singapore"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-2136-2994","authenticated-orcid":false,"given":"Ben","family":"Corden","sequence":"additional","affiliation":[{"name":"National Heart Research Institute Singapore National Heart Centre Singapore Singapore Singapore"},{"name":"Cardiovascular and Metabolic Disorders Program Duke\u2010National University of Singapore Medical School Singapore Singapore"},{"name":"MRC\u2010London Institute of Medical Sciences Hammersmith Hospital Campus London UK"},{"name":"National Heart and Lung Institute Imperial College London London UK"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Lei","family":"Ye","sequence":"additional","affiliation":[{"name":"National Heart Research Institute Singapore National Heart Centre Singapore Singapore Singapore"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Sivakumar","family":"Viswanathan","sequence":"additional","affiliation":[{"name":"Cardiovascular and Metabolic Disorders Program Duke\u2010National University of Singapore Medical School Singapore Singapore"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-9404-7608","authenticated-orcid":false,"given":"Anissa A.","family":"Widjaja","sequence":"additional","affiliation":[{"name":"Cardiovascular and Metabolic Disorders Program Duke\u2010National University of Singapore Medical School Singapore Singapore"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Chen","family":"Xie","sequence":"additional","affiliation":[{"name":"National Heart Research Institute Singapore National Heart Centre Singapore Singapore Singapore"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Liping","family":"Su","sequence":"additional","affiliation":[{"name":"National Heart Research Institute Singapore National Heart Centre Singapore Singapore Singapore"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Nicole G. 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