The cardiomyocyte molecular clock, regulation of Scn5a , and arrhythmia susceptibility
Open accessAbstract
The molecular clock mechanism underlies circadian rhythms and is defined by a transcription-translation feedback loop. Bmal1 encodes a core molecular clock transcription factor. Germline Bmal1 knockout mice show a loss of circadian variation in heart rate and blood pressure, and they develop dilated cardiomyopathy. We tested the role of the molecular clock in adult cardiomyocytes by generating mice that allow for the inducible cardiomyocyte-specific deletion of Bmal1 (iCSΔ Bmal1). ECG telemetry showed that cardiomyocyte-specific deletion of Bmal1 (iCSΔ Bmal1 −/− ) in adult mice slowed heart rate, prolonged RR and QRS intervals, and increased episodes of arrhythmia. Moreover, isolated iCSΔ Bmal1 −/− hearts were more susceptible to arrhythmia during electromechanical stimulation. Examination of candidate cardiac ion channel genes showed that Scn5a, which encodes the principle cardiac voltage-gated Na + channel (Na V 1.5), was circadianly expressed in control mouse and rat hearts but not in iCSΔ Bmal1 −/− hearts. In vitro studies confirmed circadian expression of a human Scn5a promoter-luciferase reporter construct and determined that overexpression of clock factors transactivated the Scn5a promoter. Loss of Scn5a circadian expression in iCSΔ Bmal1 −/− hearts was associated with decreased levels of Na V 1.5 and Na + current in ventricular myocytes. We conclude that disruption of the molecular clock in the adult heart slows heart rate, increases arrhythmias, and decreases the functional expression of Scn5a. These findings suggest a potential link between environmental factors that alter the cardiomyocyte molecular clock and factors that influence arrhythmia susceptibility in humans.
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Cardiomyocyte-specific deletion of Bmal1 results in loss of normal circadian expression of the Na+ and K+ channels resulting in decreased heart rate and increased risk of arrhythmias, which could contribute to sudden cardiac death.
“Cardiomyocyte-specific deletion of Bmal1 results in loss of normal circadian expression of the Na + and K + channels resulting in decreased HR and increased risk of arrhythmias (66), which could contribute to sudden cardiac death (67).”
From Role of the circadian system in cardiovascular disease (2018) · cites this paper as [66]
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- Authors
- Schroder, E. A., Lefta, M., Zhang, X., Bartos, D. C., Feng, H.-Z., Zhao, Y., Patwardhan, A., Jin, J.-P., Esser, K. A., & Delisle, B. P.
- Affiliations
- University of Kentucky (US)
- Wayne State University (US)
- Corresponding author
- Schroder, Elizabeth A.
- ORCID
- Venue
- American Journal of Physiology-Cell Physiology
- Publisher
- American Physiological Society
- Published
- 2013-05-15
- Volume
- 304
- Issue
- 10
- Pages
- C954-C965
- ISSN
- 0363-6143 (ISSN-L)
- 1522-1563
- PMC
- PMC3651636
- OpenAlex
- W2151429542
- Cited by
- 147
- References
- 59
- Citations by year
- 2026: 11 · 2025: 10 · 2024: 12 · 2023: 9 · 2022: 14 · 2021: 19 · 2020: 14 · 2019: 7 · 2018: 7 · 2017: 8 · 2016: 11 · 2015: 11 · 2014: 9 · 2013: 5
- FWCI
- 8.15
- Type
- journal article
- Language
- en
- Open access
- green
- europepmc.org
- Locations
- American Journal of Physiology-Cell Physiology (publishedVersion)
- Europe PMC (PubMed Central) (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- American Heart Association
- National Institutes of Health
- National Heart, Lung, and Blood Institute (R01HL098945, R01HL087039)
- National Institute of Environmental Health Sciences (RC1ES018636)
- National Institute of Arthritis and Musculoskeletal and Skin Diseases (R01AR055246, AR55246)
- Topics
- Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Cardiac electrophysiology and arrhythmias
- Life Sciences › Neuroscience › Endocrine and Autonomic Systems › Circadian rhythm and melatonin
- Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Cardiac pacing and defibrillation studies
- Keywords
- circadian rhythm, Bmal1, SCN5A, cardiac sodium channel, circadian gene expression, heart rate, dilated cardiomyopathy, transcription-translation feedback loop, ventricular myocytes, sodium current
- MeSH terms
- Animals, Arrhythmias, Cardiac, Biological Clocks, Blood Pressure, Cell Line, Circadian Rhythm, Heart Rate, Mice, Transgenic, Cardiomyopathies, Promoter Regions, Genetic, Rats, Inbred WKY, Gene Deletion, Myocytes, Cardiac, Mice, Rats, ARNTL Transcription Factors, NAV1.5 Voltage-Gated Sodium Channel
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