{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,21]],"date-time":"2026-09-21T10:12:35Z","timestamp":1789985555061,"version":"4.0.1"},"reference-count":42,"publisher":"Wiley","issue":"10","license":[{"start":{"date-parts":[[2011,7,22]],"date-time":"2011-07-22T00:00:00Z","timestamp":1311292800000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Journal Cellular Physiology"],"published-print":{"date-parts":[[2011,10]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:p>Cardiac hypertrophy leading to eventual heart failure is the most common cause of mortality throughout the world. The triggering mechanisms for cardiac hypertrophy are not clear but both apoptosis and cell proliferation have been reported in sections of failing hearts. In this study, we utilized both angiotensin II (AngII) treatment of cardiomyocytes and aortic ligation in rats (<jats:italic>Rattus norvegicus<\/jats:italic>, Wistar strain) for induction of hypertrophy to understand the cellular factors responsible for activation of apoptotic or anti\u2010apoptotic pathway. Hypertrophy markers (<jats:italic>ANF<\/jats:italic>, <jats:italic>\u03b2\u2010MHC<\/jats:italic>), apoptotic proteins (Bax, Bad, Fas, p53, caspase\u20103, PARP), and anti\u2010apoptotic or cell proliferation marker proteins (Bcl2, NF\u2010\u03baB, Ki\u201067) were induced significantly during hypertrophy, both in vitro as well as in vivo. Co\u2010localization of both active caspase\u20103 and Ki\u201067 was observed in hypertrophied myocytes. p53 and NF\u2010\u03baBp65 binding to co\u2010activator p300 was also increased in AngII treated myocytes. Inhibition of p53 resulted in downregulation of apoptosis, NF\u2010\u03baB activation, and NF\u2010\u03baB\u2013p300 binding; however, NF\u2010\u03baB inhibition did not inhibit apoptosis or p53\u2013p300 binding. Blocking of either p53 or NF\u2010\u03baB by specific inhibitors resulted in decrease in cell proliferation and hypertrophy markers, suggesting that p53 initially binds to p300 and then this complex recruits NF\u2010\u03baB. Thus, these results indicate the crucial role of p53 in regulating both apoptotic and cell proliferation during hypertrophy. J. Cell. Physiol. 226: 2543\u20132554, 2011. \u00a9 2010 Wiley\u2010Liss, Inc.<\/jats:p>","DOI":"10.1002\/jcp.22599","type":"journal-article","created":{"date-parts":[[2010,12,13]],"date-time":"2010-12-13T15:00:32Z","timestamp":1292252432000},"page":"2543-2554","source":"Crossref","is-referenced-by-count":52,"title":["Analysis of p53 and NF\u2010\u03baB signaling in modulating the cardiomyocyte fate during hypertrophy"],"prefix":"10.1002","volume":"226","author":[{"given":"Arunachal","family":"Chatterjee","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Saiful 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