{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,6,8]],"date-time":"2026-06-08T13:42:16Z","timestamp":1780926136043,"version":"3.54.1"},"reference-count":29,"publisher":"Oxford University Press (OUP)","issue":"1","license":[{"start":{"date-parts":[[2020,5,7]],"date-time":"2020-05-07T00:00:00Z","timestamp":1588809600000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/academic.oup.com\/journals\/pages\/open_access\/funder_policies\/chorus\/standard_publication_model"}],"funder":[{"name":"Jiangsu Provincial Youth Medical Key Talents","award":["QNRC2016431"],"award-info":[{"award-number":["QNRC2016431"]}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2020,7,1]]},"abstract":"<jats:title>Abstract<\/jats:title>\n               <jats:p\/>\n               <jats:sec>\n                  <jats:title>OBJECTIVES<\/jats:title>\n                  <jats:p>Acute myocardial infarction (AMI) is a leading cause of morbidity and mortality worldwide. Post-AMI cardiac remodelling is closely related to the prognosis of AMI. The excess inflammatory responses could promote cardiac remodelling. Tumour necrosis factor receptor-associated factor-interacting protein with forkhead-associated domain (TIFA) has been identified as a nuclear factor (NF)-\u03baB activator, which plays a key role in the activation of the NF-\u03baB signalling pathway. The goal of this research was to investigate the expression and the underlying mechanism of TIFA in an AMI mouse model.<\/jats:p>\n               <\/jats:sec>\n               <jats:sec>\n                  <jats:title>METHODS<\/jats:title>\n                  <jats:p>The AMI mouse model was induced by ligation of the left coronary artery. TIFA and NF-\u03baB knockdown were established by lentivirus transduction. The expression levels of associated proteins were analysed by a western blot or an enzyme-linked immunosorbent assay. Histological characteristics were evaluated by haematoxylin\u2013eosin staining.<\/jats:p>\n               <\/jats:sec>\n               <jats:sec>\n                  <jats:title>RESULTS<\/jats:title>\n                  <jats:p>The TIFA level was elevated in our AMI mouse model. The production of interleukin-1\u03b2 and tumour necrosis factor-\u03b1 increased markedly in the mice with AMI. TIFA knockdown inhibited the infiltration of inflammatory cells, production of pro-inflammatory mediators (interleukin-1\u03b2 and tumour necrosis factor-\u03b1), NF-\u03baB activation and cardiac remodelling (matrix metallopeptidase 9) post-AMI. In addition, NF-\u03baB knockdown could also alleviate cardiac remodelling after AMI.<\/jats:p>\n               <\/jats:sec>\n               <jats:sec>\n                  <jats:title>CONCLUSIONS<\/jats:title>\n                  <jats:p>The preceding results indicated that TIFA inhibition could ameliorate cardiac remodelling after AMI partly through inactivation of NF-\u03baB. This study provides insights into further research of cardiac remodelling and AMI from bench to clinic.<\/jats:p>\n               <\/jats:sec>","DOI":"10.1093\/icvts\/ivaa060","type":"journal-article","created":{"date-parts":[[2020,3,17]],"date-time":"2020-03-17T12:17:23Z","timestamp":1584447443000},"page":"85-92","source":"Crossref","is-referenced-by-count":3,"title":["Tumour necrosis factor receptor-associated factors: interacting protein with forkhead-associated domain inhibition decreases inflammatory cell infiltration and cardiac remodelling after acute myocardial infarction"],"prefix":"10.1093","volume":"31","author":[{"given":"Yicheng","family":"Jiang","sequence":"first","affiliation":[{"name":"Department of Cardiology, Huai\u2019an First People\u2019s Hospital, Nanjing Medical University, Huai\u2019an, Jiangsu, China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Xue","family":"Li","sequence":"first","affiliation":[{"name":"Department of Heart Disease, 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