ArticleJCI insight2019
Muscarinic receptors promote pacemaker fate at the expense of secondary conduction system tissue in zebrafish.
Article in JCI insight, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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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.
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Who cites it
13 citing papers in PubMed, 28 citations in OpenAlex.
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- Identification and Validation of Genes Exhibiting Dynamic Alterations in Response to Bleomycin-Induced Pulmonary Fibrosis.Molecular biotechnology · 2024Article
- Macrophage-enriched novel functional long noncoding RNAs LRRC75A-AS1 and GAPLINC regulate polarization and innate immune responses.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2024Article
- Pathophysiology and pharmacology of G protein-coupled receptors in the heart.Cardiovascular research · 2023Review
- Semaphorin3f as a cardiomyocyte derived regulator of heart chamber development.Cell communication and signaling : CCS · 2022Article
- Zebrafish disease models in drug discovery: from preclinical modelling to clinical trials.Nature reviews. Drug discovery · 2021Review
- Zebrafish Heart Failure Models.Frontiers in cell and developmental biology · 2021Review
- Fibroblast Growth Factor (FGF) 13.Differentiation; research in biological diversityReview
Corrections and comments
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Authors and funding
19 authors at 5 institutions in 4 countries.
Funding
Abstract
Deterioration or inborn malformations of the cardiac conduction system (CCS) interfere with proper impulse propagation in the heart and may lead to sudden cardiac death or heart failure. Patients afflicted with arrhythmia depend on antiarrhythmic medication or invasive therapy, such as pacemaker implantation. An ideal way to treat these patients would be CCS tissue restoration. This, however, requires precise knowledge regarding the molecular mechanisms underlying CCS development. Here, we aimed to identify regulators of CCS development. We performed a compound screen in zebrafish embryos and identified tolterodine, a muscarinic receptor antagonist, as a modifier of CCS development. Tolterodine provoked a lower heart rate, pericardiac edema, and arrhythmia. Blockade of muscarinic M3, but not M2, receptors induced transcriptional changes leading to amplification of sinoatrial cells and loss of atrioventricular identity. Transcriptome data from an engineered human heart muscle model provided additional evidence for the contribution of muscarinic M3 receptors during cardiac progenitor specification and differentiation. Taken together, we found that muscarinic M3 receptors control the CCS already before the heart becomes innervated. Our data indicate that muscarinic receptors maintain a delicate balance between the developing sinoatrial node and the atrioventricular canal, which is probably required to prevent the development of arrhythmia.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.