ArticleJournal of comparative physiology. B, Biochemical, systemic, and environmental physiology2017
Melatonin increases the regularity of cardiac rhythmicity in the Drosophila heart in both wild-type and strains bearing pathogenic mutations.
Article in Journal of comparative physiology. B, Biochemical, systemic, and environmental physiology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 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.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
3 citing papers in PubMed, 10 citations in OpenAlex.
- Smoking flies: testing the effect of tobacco cigarettes on heart function ofBiology open · 2021Article
- Using optogenetics to assess neuroendocrine modulation of heart rate in Drosophila melanogaster larvae.Journal of comparative physiology. A, Neuroethology, sensory, neural, and behavioral physiology · 2017Article
- Dietary Sources and Bioactivities of Melatonin.Nutrients · 2017Review
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Melatonin is a hormone that is critical for normal circadian and seasonal rhythmicity in a wide range of different animals. It is a powerful antioxidant commonly used to prevent reperfusion injury to the heart after infarction. We show here it has other more far-reaching effects on cardiac function. Using the Drosophila model, we show that injection of melatonin increases the regularity of heartbeat significantly and can rescue rhythmicity in flies bearing mutations that adversely affect cardiac function. Notably, melatonin increases cardiac regularity independent of alteration of heart rate. We provide compelling evidence that melatonin's action as an antioxidant is not the mechanism underlying improved cardiac performance. We have strong evidence that melatonin's action on the heart is mediated via a specific G-Protein-coupled receptor encoded by the CG 4313 gene that our results implicate as a candidate melatonin receptor. These results open a line of questioning about fundamental aspects of cardiac pacemaking.
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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.