ArticleCirculation. Arrhythmia and electrophysiology2010
Absence of the inhibitory G-protein Galphai2 predisposes to ventricular cardiac arrhythmia.
Article in Circulation. Arrhythmia and electrophysiology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 26 citations in OpenAlex.
- The Orally Available Ghrelin Receptor-Agonist AC01 Improves Systolic Function in HFrEF Mice and Nonhuman Primates.JACC. Basic to translational science · 2026Article
- Single-Cell Genomics and Somatic Variation in Circulating and Cardiac Resident Cells.Circulation research · 2026Review
- The ric-8b protein (resistance to inhibitors of cholinesterase 8b) is key to preserving contractile function in the adult heart.The Journal of biological chemistry · 2024Article
- Somatic Mutations in Cardiovascular Disease.Circulation research · 2022Review
- Analyses of Gnai3-iresGFP reporter mice reveal unknown GαScientific reports · 2021Article
- Differential effects of inhibitory G protein isoforms on G protein-gated inwardly rectifying KAmerican journal of physiology. Cell physiology · 2018Article
- A modified approach for programmed electrical stimulation in mice: Inducibility of ventricular arrhythmias.PloS one · 2018Article
- Tissue-Level Cardiac Electrophysiology Studied in Murine Myocardium Using a Microelectrode Array: Autonomic and Thermal Modulation.The Journal of membrane biology · 2017Article
- Correlation of Ventricular Arrhythmogenesis with Neuronal Remodeling of Cardiac Postganglionic Parasympathetic Neurons in the Late Stage of Heart Failure after Myocardial Infarction.Frontiers in neuroscience · 2017Article
- Have the Findings from Clinical Risk Prediction and Trials Any Key Messages for Safety Pharmacology?Frontiers in physiology · 2017Review
- Blunted apoptosis of erythrocytes in mice deficient in the heterotrimeric G-protein subunit Gαi2.Scientific reports · 2016Article
- The role of GαO-mediated signaling in the rostral ventrolateral medulla oblongata in cardiovascular reflexes and control of cardiac ventricular excitability.Physiological reports · 2016Article
- Control of ventricular excitability by neurons of the dorsal motor nucleus of the vagus nerve.Heart rhythm · 2015Article
- Absence of the Regulator of G-protein Signaling, RGS4, Predisposes to Atrial Fibrillation and Is Associated with Abnormal Calcium Handling.The Journal of biological chemistry · 2015Article
- Circulating Cell and Plasma microRNA Profiles Differ between Non-ST-Segment and ST-Segment-Elevation Myocardial Infarction.Family medicine & medical science research · 2013Article
- Essential role of the m2R-RGS6-IKACh pathway in controlling intrinsic heart rate variability.PloS one · 2013Article
- The Role of Inhibitory G Proteins and Regulators of G Protein Signaling in the in vivo Control of Heart Rate and Predisposition to Cardiac Arrhythmias.Frontiers in physiology · 2012Article
- Gαi2- and Gαi3-specific regulation of voltage-dependent L-type calcium channels in cardiomyocytes.PloS one · 2011Article
Corrections and comments
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Authors and funding
8 authors at 1 institution in 2 countries.
Funding
Abstract
backgroundWe explored the role that inhibitory heterotrimeric G-proteins play in ventricular arrhythmia. METHODS AND
resultsMice with global genetic deletion of Galpha(i2) [Galpha(i2) (-/-)] were studied and found, based on telemetry, to have a prolonged QT interval on surface ECG when awake. In vivo electrophysiology studies revealed that the Galpha(i2) (-/-) mice have a reduced ventricular effective refractory period and a predisposition to ventricular tachycardia when challenged with programmed electrical stimulation. Neither control nor combined global deletion of Galpha(i1) and Galpha(i3) mice showed these abnormalities. There was no evidence for structural heart disease at this time point in the Galpha(i2) (-/-) mice as assessed by cardiac histology and echocardiography. The absence of Galpha(i2) thus leads to a primary electrical abnormality, and we explored the basis for this finding. With patch clamping, single isolated ventricular cells showed that Galpha(i2) (-/-) mice had a prolonged ventricular action potential duration (APD) but steeper action potential shortening as the diastolic interval was reduced in restitution studies. Gene expression studies showed increased expression of L-type Ca(2+) channel subunits, and patch clamping revealed an increase in these currents in Galpha(i2) (-/-) mice. There were no changes in K(+) currents.
conclusionsThe absence of inhibitory G-protein signaling mediated through Galpha(i2) is a substrate for ventricular arrhythmias.
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