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In the present study, a <jats:italic>Tnni3k<\/jats:italic> cardiomyocyte\u2010specific knockout (<jats:italic>Tnni3k<\/jats:italic>\u2010cKO) mouse model was established. Echocardiography was used to evaluate cardiac function in mice. Heart failure markers were detected using enzyme\u2010linked immunosorbent assay. Haematoxylin and eosin staining, wheat germ agglutinin staining, Masson's trichrome staining, Sirius red staining and terminal deoxynucleotidyl transferase dUTP nick end labelling (TUNEL) staining were used to assess histopathological changes, cardiac hypertrophy, collagen deposition and myocardial apoptosis, respectively. Expression levels of TNNI3K, apoptosis\u2010related proteins, and p38 mitogen\u2010activated protein kinase were measured using Western blot analysis. Compared to wild\u2010type controls, cardiac dysfunction and cardiac remodelling of <jats:italic>Tnni3k<\/jats:italic>\u2010cKO mice increased gradually with age. <jats:italic>Tnni3k<\/jats:italic>\u2010cKO mice exhibited cardiac hypertrophy, cardiac fibrosis and cardiomyocyte apoptosis. Upregulation of cleaved caspase\u20103 in <jats:italic>Tnni3k<\/jats:italic>\u2010cKO mice appeared to be related to phosphorylation and activation of the p38 mitogen\u2010activated protein kinase signalling pathway. In conclusion, this study shows that TNNI3K is essential for cardiac development and function, providing new insights into the development of novel therapeutic strategies for cardiac diseases.<\/jats:p>","DOI":"10.1111\/1440-1681.13699","type":"journal-article","created":{"date-parts":[[2022,7,4]],"date-time":"2022-07-04T08:08:59Z","timestamp":1656922139000},"page":"1169-1178","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":2,"title":["Knockout of cardiac troponin <scp>I\u2010interacting<\/scp> kinase leads to cardiac dysfunction and remodelling"],"prefix":"10.1111","volume":"49","author":[{"given":"Huilin","family":"Qu","sequence":"first","affiliation":[{"name":"State Key Laboratory of Cardiovascular Disease, National Center for Cardiovascular Disease, Fu Wai Hospital Chinese Academy of Medical Sciences and Peking Union Medical College  Beijing 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