{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,13]],"date-time":"2026-10-13T16:40:18Z","timestamp":1791909618909,"version":"4.3.4"},"reference-count":36,"publisher":"Wiley","issue":"5","license":[{"start":{"date-parts":[[2007,1,31]],"date-time":"2007-01-31T00:00:00Z","timestamp":1170201600000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"},{"start":{"date-parts":[[2007,1,31]],"date-time":"2007-01-31T00:00:00Z","timestamp":1170201600000},"content-version":"tdm","delay-in-days":0,"URL":"http:\/\/doi.wiley.com\/10.1002\/tdm_license_1.1"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["J of Cellular Biochemistry"],"published-print":{"date-parts":[[2007,4,1]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:p>\n                    Recent in vitro studies suggest that adenosine monophosphate (AMP)\u2010activated protein kinase (AMPK) exerts inhibitory effects on cardiac hypertrophy. However, it is unclear whether long\u2010term activation of AMPK will affect cardiac hypertrophy in vivo. In these reports, we investigate the in vivo effects of long\u2010term AMPK activation on cardiac hypertrophy and the related molecular mechanisms. To examine the effects of AMPK activation in the development of pressure overload\u2010induced cardiac hypertrophy, we administered 5\u2010aminoimidazole 1 carboxamide ribonucleoside (AICAR, 0.5 mg\/g body wt), a specific activator of AMPK, to rats with transaortic constriction (TAC) for 7 weeks. We found that long\u2010term AMPK activation attenuated cardiac hypertrophy, and improved cardiac function in rats subjected to TAC. Furthermore, long\u2010term AMPK activation attenuated protein synthesis, diminished calcineurin\u2010nuclear factor of activated T cells (NFAT) and nuclear factor \u03baB (NF\u2010\u03baB) signaling in pressure overload\u2010induced hypertrophic hearts. Our in vitro experiments further proved that activation of AMPK by infection of AdAMPK blocked cardiac hypertrophy and NFAT, NF\u2010\u03baB, and MAPK signal pathways. The present study demonstrates for the first time that pharmacological activation of AMPK inhibits cardiac hypertrophy\n                    <jats:italic>in<\/jats:italic>\n                    through blocking signaling transduction pathways that are involved in cardiac growth. It presents a potential therapy strategy to inhibit pathological cardiac hypertrophy by increasing the activity of AMPK. J. Cell. Biochem. 100: 1086\u20131099, 2007. \u00a9 2007 Wiley\u2010Liss, Inc.\n                  <\/jats:p>","DOI":"10.1002\/jcb.21197","type":"journal-article","created":{"date-parts":[[2007,2,3]],"date-time":"2007-02-03T00:28:04Z","timestamp":1170462484000},"page":"1086-1099","source":"Crossref","is-referenced-by-count":113,"title":["Long\u2010term activation of adenosine monophosphate\u2010activated protein kinase attenuates pressure\u2010overload\u2010induced cardiac 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