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We demonstrate that miR-155 expressed in cardiac fibroblasts is a potent contributor to cardiac remodeling. We reveal that in vivo, miR-155 knockout improves left ventricular function, reduces infarct size, and attenuates collagen deposition, whereas overexpression of miR-155 produces the opposite effects. MiR-155 knockout also inhibits cardiac fibroblast proliferation and differentiation into myofibroblasts. In addition, downregulation of tumor protein p53-inducible nuclear protein 1 (TP53INP1) by small interfering RNA reverses the effects of miR-155 knockout on cardiac fibroblasts. Our data reveal that knockout of miR-155 in cardiac fibroblasts improves cardiac remodeling by targeting TP53INP1, which may be a novel treatment strategy for cardiac remodeling.<\/jats:p>","DOI":"10.1177\/1074248415616188","type":"journal-article","created":{"date-parts":[[2015,11,20]],"date-time":"2015-11-20T21:49:45Z","timestamp":1448056185000},"page":"423-435","update-policy":"https:\/\/doi.org\/10.1177\/sage-journals-update-policy","source":"Crossref","is-referenced-by-count":53,"title":["MiR-155 Knockout in Fibroblasts Improves Cardiac Remodeling by Targeting Tumor Protein p53-Inducible Nuclear Protein 1"],"prefix":"10.1177","volume":"21","author":[{"given":"Wangwei","family":"He","sequence":"first","affiliation":[{"name":"Department of Cardiology, Renmin Hospital of Wuhan University, Wuhan, PR China"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"He","family":"Huang","sequence":"additional","affiliation":[{"name":"Department of Cardiology, Renmin Hospital of 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