| Article ID | Journal | Published Year | Pages | File Type |
|---|---|---|---|---|
| 10763646 | Biochemical and Biophysical Research Communications | 2011 | 6 Pages |
Abstract
⺠Diacylglycerol-activated TRPC3 channels are up-regulated in dilated cardiomyopathy. ⺠Activation of TRPC3 increases Ca2+/calmodulin-dependent kinase activity. ⺠Inhibition of TRPC3 attenuates the progression of dilated cardiomyopathy. ⺠Inhibition of TRPC3 also suppresses production of reactive oxygen species. ⺠TRPC3-mediated Ca2+ influx contributes to NADPH oxidase activation in rodent cardiomyocytes.
Keywords
4-HNEβARK1-Oleoyl-2-acetyl-sn-glycerolMuscle LIM proteinLTCCsβAROAGAT1RPKCdichlorofluoresceinCaMKIIDPINFATDcfMLPDCM4-hydroxy-2-nonenalCa2+/Calmodulin-dependent kinase IINOxangiotensinNADPH oxidaseAngleft ventricledihydroethidiumdiacylglycerolDiphenyleneiodoniumDAGNuclear Factor of Activated T CellsDHEProtein kinase CDilated cardiomyopathyL-type Ca2+ channelsβ adrenergic receptor
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Authors
Naoyuki Kitajima, Kunihiro Watanabe, Sachio Morimoto, Yoji Sato, Shigeki Kiyonaka, Masahiko Hoshijima, Yasuhiro Ikeda, Michio Nakaya, Tomomi Ide, Yasuo Mori, Hitoshi Kurose, Motohiro Nishida,