{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,1,21]],"date-time":"2026-01-21T11:39:34Z","timestamp":1768995574025,"version":"3.49.0"},"reference-count":34,"publisher":"American Physiological Society","issue":"6","funder":[{"DOI":"10.13039\/501100000274","name":"British Heart Foundation (BHF)","doi-asserted-by":"publisher","award":["CH\/11\/3\/29051"],"award-info":[{"award-number":["CH\/11\/3\/29051"]}],"id":[{"id":"10.13039\/501100000274","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100000274","name":"British Heart Foundation (BHF)","doi-asserted-by":"publisher","award":["RG\/11\/12\/29052"],"award-info":[{"award-number":["RG\/11\/12\/29052"]}],"id":[{"id":"10.13039\/501100000274","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100000274","name":"British Heart Foundation (BHF)","doi-asserted-by":"publisher","award":["RE\/13\/2\/30182"],"award-info":[{"award-number":["RE\/13\/2\/30182"]}],"id":[{"id":"10.13039\/501100000274","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100001691","name":"Japan Society for the Promotion of Science (JSPS)","doi-asserted-by":"publisher","award":["15H04822"],"award-info":[{"award-number":["15H04822"]}],"id":[{"id":"10.13039\/501100001691","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Heart and Circulatory Physiology"],"published-print":{"date-parts":[[2016,12,1]]},"abstract":"<jats:p>We have reported that the Toll-like receptor 9 (TLR9) signaling pathway plays an important role in the development of pressure overload-induced inflammatory responses and heart failure. However, its role in cardiac remodeling after myocardial infarction has not been elucidated. TLR9-deficient and control C57Bl\/6 wild-type mice were subjected to left coronary artery ligation. The survival rate 14 days postoperation was significantly lower in TLR9-deficient mice than that in wild-type mice with evidence of cardiac rupture in all dead mice. Cardiac magnetic resonance imaging showed no difference in infarct size and left ventricular wall thickness and function between TLR9-deficient and wild-type mice. There were no differences in the number of infiltrating inflammatory cells and the levels of inflammatory cytokine mRNA in infarct hearts between TLR9-deficient and wild-type mice. The number of \u03b1-smooth muscle actin (\u03b1SMA)-positive myofibroblasts and \u03b1SMA\/Ki67-double-positive proliferative myofibroblasts was increased in the infarct and border areas in infarct hearts compared with those in sham-operated hearts in wild-type mice, but not in TLR9-deficient mice. The class B CpG oligonucleotide increased the phosphorylation level of NF-\u03baB and the number of \u03b1SMA-positive and \u03b1SMA\/Ki67-double-positive cells and these increases were attenuated by BAY1-7082, an NF-\u03baB inhibitor, in cardiac fibroblasts isolated from wild-type hearts. The CpG oligonucleotide showed no effect on NF-\u03baB activation or the number of \u03b1SMA-positive and \u03b1SMA\/Ki67-double-positive cells in cardiac fibroblasts from TLR9-deficient hearts. Although the TLR9 signaling pathway is not involved in the acute inflammatory response in infarct hearts, it ameliorates cardiac rupture possibly by promoting proliferation and differentiation of cardiac fibroblasts.<\/jats:p><jats:p>Listen to this article\u2019s corresponding podcast @ http:\/\/ajpheart.podbean.com\/e\/tlr9-in-post-infarct-cardiac-rupture\/ .<\/jats:p>","DOI":"10.1152\/ajpheart.00481.2016","type":"journal-article","created":{"date-parts":[[2016,10,22]],"date-time":"2016-10-22T03:45:43Z","timestamp":1477107943000},"page":"H1485-H1497","source":"Crossref","is-referenced-by-count":42,"title":["Toll-like receptor 9 prevents cardiac rupture after myocardial infarction in mice independently of inflammation"],"prefix":"10.1152","volume":"311","author":[{"given":"Shigemiki","family":"Omiya","sequence":"first","affiliation":[{"name":"Cardiovascular Division, King\u2019s College London British Heart Foundation Centre of Research Excellence, London, United Kingdom;"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Yosuke","family":"Omori","sequence":"additional","affiliation":[{"name":"Cardiovascular Division, King\u2019s College London British Heart Foundation Centre of Research Excellence, London, United Kingdom;"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Manabu","family":"Taneike","sequence":"additional","affiliation":[{"name":"Cardiovascular Division, King\u2019s College London British Heart Foundation Centre of Research Excellence, London, United Kingdom;"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Andrea","family":"Protti","sequence":"additional","affiliation":[{"name":"Cardiovascular Division, King\u2019s College London British Heart Foundation Centre of Research Excellence, London, United Kingdom;"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Osamu","family":"Yamaguchi","sequence":"additional","affiliation":[{"name":"Department of Cardiovascular Medicine, Osaka University Graduate School of Medicine, Suita, Japan; 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