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. 2013 Dec 17;10(1):64–72. doi: 10.7150/ijbs.7894

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© Ivyspring International Publisher. This is an open-access article distributed under the terms of the Creative Commons License (http://creativecommons.org/licenses/by-nc-nd/3.0/). Reproduction is permitted for personal, noncommercial use, provided that the article is in whole, unmodified, and properly cited.

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Proposed mechanisms of KMUP-1 modulation of serotonin-induced hypertrophic H9c2 cardiomyocytes involving the protein kinase cascade. Serotonin-induced H9c2 cell hypertrophy was reversed by the K⁺ channel opener KMUP-1, attenuated by the LTCC blocker verapamil and the 5-HT_2A antagonist ketanserin, but unaffected by the 5-HT_2B antagonist SB206553. Collectively, serotonin-increased I_Ca,L could be mainly due to activated 5-HT_2A receptor-mediated PKA and PKC cascades, and partly attributed to interaction with PKG. Accordingly, KMUP-1 blocks serotonin-induced H9c2 hypertrophy, which can be attributed to its PKA and PKC inhibition or PKG stimulation.