Phosphoinositide 3-kinase γ protects against catecholamine-induced ventricular arrhythmia through protein kinase A-mediated regulation of distinct phosphodiesterases.

@article{Ghigo2012Phosphoinositide3,
  title={Phosphoinositide 3-kinase γ protects against catecholamine-induced ventricular arrhythmia through protein kinase A-mediated regulation of distinct phosphodiesterases.},
  author={Alessandra Ghigo and Alessia Perino and Hind Mehel and Alexandra Zahradn{\'i}kov{\'a} and Fulvio Morello and J{\'e}r{\^o}me Leroy and Viacheslav O Nikolaev and Federico Damilano and James I Cimino and Elisa De Luca and Wito Richter and Ruth E. Westenbroek and William A. Catterall and Jin Zhang and Chen Yan and M. P{\'e}rez-D{\'i}az Conti and Ana M G{\'o}mez and Gr{\'e}goire Vandecasteele and Emilio Hirsch and Rodolphe Fischmeister},
  journal={Circulation},
  year={2012},
  volume={126 17},
  pages={2073-83}
}
BACKGROUND Phosphoinositide 3-kinase γ (PI3Kγ) signaling engaged by β-adrenergic receptors is pivotal in the regulation of myocardial contractility and remodeling. However, the role of PI3Kγ in catecholamine-induced arrhythmia is currently unknown. METHODS AND RESULTS Mice lacking PI3Kγ (PI3Kγ(-/-)) showed runs of premature ventricular contractions on adrenergic stimulation that could be rescued by a selective β(2)-adrenergic receptor blocker and developed sustained ventricular tachycardia… CONTINUE READING
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