title: The contribution of pathways initiated via the Gq\11 G-protein family to atrial fibrillation.
abstract: Atrial fibrillation is the commonest cardiac arrhythmia and leads to significant clinical morbidity and mortality. It has a complex pathophysiology but is often initiated by atrial ectopic beats and because of atrial remodelling once it occurs it can become established. Thus therapeutic interventions designed to prevent the initial occurrence of the arrhythmia are particularly needed. At the cellular level, these ectopic beats arise because of abnormal calcium release events from the sarcoplasmic reticulum leading to an inward current mediated by the sodium-calcium exchanger. There has been considerable interest in this over the last few years largely focused on the ryanodine receptor and related signalling pathways. However, atrial myocytes also possess a well-developed inositol trisphosphate (IP3) dependent calcium release system and this has been less studied. In this review we focus on pathways and molecules that couple via the Gq\11 family of G-proteins including regulators of G-protein signalling that may influence IP3 mediated calcium release and atrial fibrillation.
authors.affiliation: The Heart Centre, William Harvey Research Institute, Barts and the London School of Medicine and Dentistry, Charterhouse Square, London EC1M6BQ, UK. Electronic address: a.tinker@qmul.ac.uk.
authors.forename: Andrew
authors.initials: A
authors.lastname: Tinker
authors.affiliation: The Heart Centre, William Harvey Research Institute, Barts and the London School of Medicine and Dentistry, Charterhouse Square, London EC1M6BQ, UK.
authors.forename: Malcom
authors.initials: M
authors.lastname: Finlay
authors.affiliation: The Heart Centre, William Harvey Research Institute, Barts and the London School of Medicine and Dentistry, Charterhouse Square, London EC1M6BQ, UK.
authors.forename: Muriel
authors.initials: M
authors.lastname: Nobles
authors.affiliation: The Heart Centre, William Harvey Research Institute, Barts and the London School of Medicine and Dentistry, Charterhouse Square, London EC1M6BQ, UK.
authors.forename: Aaisha
authors.initials: A
authors.lastname: Opel
mesh_terms: D000818:Animals; D001281:Atrial Fibrillation / Q000188:drug therapy / Q000378:metabolism* / Q000473:pathology; D002118:Calcium / Q000378:metabolism*; D055808:Drug Discovery; D043802:GTP-Binding Protein alpha Subunits, Gq-G11 / Q000378:metabolism*; D006325:Heart Atria / Q000187:drug effects / Q000378:metabolism / Q000473:pathology; D006801:Humans; D007295:Inositol Phosphates / Q000378:metabolism*; D058990:Molecular Targeted Therapy; D032383:Myocytes, Cardiac / Q000187:drug effects / Q000378:metabolism / Q000473:pathology; D019837:Ryanodine Receptor Calcium Release Channel / Q000378:metabolism; D015398:Signal Transduction / Q000187:drug effects
chemical_list: D007295:Inositol Phosphates; D019837:Ryanodine Receptor Calcium Release Channel; C516441:inositol trispyrophosphate; D043802:GTP-Binding Protein alpha Subunits, Gq-G11; D002118:Calcium
keywords: Atrial fibrillation; Calcium; Cardiac arrhythmia; G-protein; Gq\11; IP3; Regulators of G-protein signalling