{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,2]],"date-time":"2026-09-02T06:17:19Z","timestamp":1788329839659,"version":"build-2803163510"},"reference-count":49,"publisher":"Wiley","issue":"8","license":[{"start":{"date-parts":[[2020,3,10]],"date-time":"2020-03-10T00:00:00Z","timestamp":1583798400000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["J Cellular Molecular Medi"],"published-print":{"date-parts":[[2020,4]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:p>Myocardial infarction (MI) is an acute coronary syndrome that refers to tissue infarction of the myocardium. This study aimed to investigate the effect of long intergenic non\u2010protein\u2010coding RNA (lincRNA) ATPase plasma membrane Ca<jats:sup>2+<\/jats:sup> transporting 1 antisense RNA 1 (ATP2B1\u2010AS1) against MI by targeting nuclear factor\u2010kappa\u2010B inhibitor alpha (NFKBIA) and mediating the nuclear factor\u2010kappa\u2010B (NF\u2010\u03baB) signalling pathway. An MI mouse model was established and idenepsied by cardiac function evaluation. It was determined that ATP2B1\u2010AS1 was highly expressed, while NFKBIA was poorly expressed and NF\u2010\u03baB signalling pathway was activated in MI mice. Cardiomyocytes were extracted from mice and introduced with a series of mouse ATP2B1\u2010AS1 vector, NFKBIA vector, siRNA\u2010mouse ATP2B1\u2010AS1 and siRNA\u2010NFKBIA. The expression of NF\u2010\u03baBp50, NF\u2010\u03baBp65 and IKK\u03b2 was determined to idenepsy whether ATP2B1\u2010AS1 and NFKBIA affect the NF\u2010\u03baB signalling pathway, the results of which suggested that ATP2B1\u2010AS1 down\u2010regulated the expression of NFKBIA and activated the NF\u2010\u03baB signalling pathway in MI mice. Based on the data from assessment of cell viability, cell cycle, apoptosis and levels of inflammatory cytokines, either silencing of mouse ATP2B1\u2010AS1 or overexpression of NFKBIA was suggested to result in reduced cardiomyocyte apoptosis and expression of inflammatory cytokines, as well as enhanced cardiomyocyte viability. Our study provided evidence that mouse ATP2B1\u2010AS1 silencing may have the potency to protect against MI in mice through inhibiting cardiomyocyte apoptosis and inflammation, highlighting a great promise as a novel therapeutic target for MI.<\/jats:p>","DOI":"10.1111\/jcmm.15105","type":"journal-article","created":{"date-parts":[[2020,3,10]],"date-time":"2020-03-10T20:10:09Z","timestamp":1583871009000},"page":"4466-4479","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":34,"title":["Silencing of ATP2B1\u2010AS1 contributes to protection against myocardial infarction in mouse via blocking NFKBIA\u2010mediated NF\u2010\u03baB signalling pathway"],"prefix":"10.1111","volume":"24","author":[{"given":"Kai\u2010You","family":"Song","sequence":"first","affiliation":[{"name":"Department of Cardiology Linyi People's Hospital Linyi 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