Cardiac arrhythmia induced by genetic silencing of ‘funny’ (f) channels is rescued by GIRK4 inactivation View Full Text


Ontology type: schema:ScholarlyArticle      Open Access: True


Article Info

DATE

2014-12

AUTHORS

Pietro Mesirca, Jacqueline Alig, Angelo G. Torrente, Jana Christina Müller, Laurine Marger, Anne Rollin, Claire Marquilly, Anne Vincent, Stefan Dubel, Isabelle Bidaud, Anne Fernandez, Anika Seniuk, Birgit Engeland, Jasmin Singh, Lucile Miquerol, Heimo Ehmke, Thomas Eschenhagen, Joel Nargeot, Kevin Wickman, Dirk Isbrandt, Matteo E. Mangoni

ABSTRACT

The mechanisms underlying cardiac automaticity are still incompletely understood and controversial. Here we report the complete conditional and time-controlled silencing of the 'funny' current (If) by expression of a dominant-negative, non-conductive HCN4-channel subunit (hHCN4-AYA). Heart-specific If silencing caused altered [Ca(2+)]i release and Ca(2+) handling in the sinoatrial node, impaired pacemaker activity and symptoms reminiscent of severe human disease of pacemaking. The effects of If silencing critically depended on the activity of the autonomic nervous system. We were able to rescue the failure of impulse generation and conduction by additional genetic deletion of cardiac muscarinic G-protein-activated (GIRK4) channels in If-deficient mice without impairing heartbeat regulation. Our study establishes the role of f-channels in cardiac automaticity and indicates that arrhythmia related to HCN loss-of-function may be managed by pharmacological or genetic inhibition of GIRK4 channels, thus offering a new therapeutic strategy for the treatment of heart rhythm diseases. More... »

PAGES

4664

Identifiers

URI

http://scigraph.springernature.com/pub.10.1038/ncomms5664

DOI

http://dx.doi.org/10.1038/ncomms5664

DIMENSIONS

https://app.dimensions.ai/details/publication/pub.1052839045

PUBMED

https://www.ncbi.nlm.nih.gov/pubmed/25144323


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