ArticleScientific reports2023
Increased GIRK channel activity prevents arrhythmia in mice with heart failure by enhancing ventricular repolarization.
Article in Scientific reports, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
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Who cites it
5 citing papers in PubMed, 5 citations in OpenAlex.
- The p.Arg52Leu variant in GNB2 causes a gain-of-function due to an increase of IBMC cardiovascular disorders · 2026Article
- Autonomic imbalance in cardiovascular disease: molecular mechanisms and emerging therapeutics.American journal of physiology. Cell physiology · 2025Review
- Global but not myeloid lineage-directed Girk3 deletion increases bone mass in female mice.JBMR plus · 2025Article
- Review
- Direct modulation of G protein-gated inwardly rectifying potassium (GIRK) channels.Frontiers in physiology · 2024Review
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Authors and funding
2 authors at 2 institutions in 2 countries.
Funding
Abstract
Ventricular arrhythmia causing sudden cardiac death is the leading mode of death in patients with heart failure. Yet, the mechanisms that prevent ventricular arrhythmias in heart failure are not well characterized. Using a mouse model of heart failure created by transverse aorta constriction, we show that GIRK channel, an important regulator of cardiac action potentials, is constitutively active in failing ventricles in contrast to normal cells. Evidence is presented indicating that the tonic activation of M
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Registered trials
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