Open AccessCalmodulin/CaMKII inhibition improves intercellular communication and impulse propagation in the heart and is antiarrhythmic under conditions when fibrosis is absent
Author(s) -
Hiroki Takanari,
Vincent J.A. Bourgonje,
Magda S. C. Fontes,
A. Raaijmakers,
Helen E. Driessen,
John A. Jansen,
Roel van der Nagel,
Bart Kok,
Leonie van Stuijvenberg,
M. Boulaksil,
Yoshio Takemoto,
Masatoshi Yamazaki,
Yukiomi Tsuji,
Haruo Honjo,
Kaichiro Kamiya,
Itsuo Kodama,
Mark E. Anderson,
Marcel A. G. van der Heyden,
Harold V.M. van Rijen,
Toon A.B. van Veen,
Marc A. Vos
Publication year - 2016
Publication title -
cardiovascular research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.774
H-Index - 219
eISSN - 1755-3245
pISSN - 0008-6363
DOI - 10.1093/cvr/cvw173
Subject(s) - calmodulin , gap junction , intracellular , chemistry , medicine , endocrinology , optical mapping , calcium , biochemistry
In healthy hearts, ventricular gap junctions are mainly composed by connexin43 (Cx43) and localize in the intercalated disc, enabling appropriate electrical coupling. In diseased hearts, Cx43 is heterogeneously down-regulated, whereas activity of calmodulin/calcium-calmodulin protein kinase II (CaM/CaMKII) signalling increases. It is unclear if CaM/CaMKII affects Cx43 expression/localization or impulse propagation. We analysed different models to assess this.
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