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Development of dilated cardiomyopathy in Bmal1-deficient mice
Open accessAbstract
Circadian rhythms are approximate 24-h oscillations in physiology and behavior. Circadian rhythm disruption has been associated with increased incidence of hypertension, coronary artery disease, dyslipidemia, and other cardiovascular pathologies in both humans and animal models. Mice lacking the core circadian clock gene, brain and muscle aryl hydrocarbon receptor nuclear translocator (ARNT)-like protein ( Bmal1), are behaviorally arrhythmic, die prematurely, and display a wide range of organ pathologies. However, data are lacking on the role of Bmal1 on the structural and functional integrity of cardiac muscle. In the present study, we demonstrate that Bmal1−/−mice develop dilated cardiomyopathy with age, characterized by thinning of the myocardial walls, dilation of the left ventricle, and decreased cardiac performance. Shortly after birth the Bmal1−/−mice exhibit a transient increase in myocardial weight, followed by regression and later onset of dilation and failure. Ex vivo working heart preparations revealed systolic ventricular dysfunction at the onset of dilation and failure, preceded by downregulation of both myosin heavy chain isoform mRNAs. We observed structural disorganization at the level of the sarcomere with a shift in titin isoform composition toward the stiffer N2B isoform. However, passive tension generation in single cardiomyocytes was not increased. Collectively, these findings suggest that the loss of the circadian clock gene, Bmal1, gives rise to the development of an age-associated dilated cardiomyopathy, which is associated with shifts in titin isoform composition, altered myosin heavy chain gene expression, and disruption of sarcomere structure.
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“For instance, Bmal1 knockout in mice causes dilated cardiomyopathy (62) and selective Bmal1 knockout in cardiomyocytes eliminates much of the rhythmic transcriptome (63), reduces stroke volume and ejection fraction, and causes heart failure and early mortality in mice (63,64).”
From Role of the circadian system in cardiovascular disease (2018) · cites this paper as [62]
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Metadata
- Authors
- Lefta, M., Campbell, K. S., Feng, H.-Z., Jin, J.-P., & Esser, K. A.
- Affiliations
- University of Kentucky (US)
- Wayne State University (US)
- Corresponding author
- Esser, Karyn A.
- Venue
- American Journal of Physiology-Heart and Circulatory Physiology
- Publisher
- American Physiological Society
- Published
- 2012-08-15
- Volume
- 303
- Issue
- 4
- Pages
- H475-H485
- ISSN
- 0363-6135 (ISSN-L)
- 1522-1539
- PMC
- PMC3423146
- OpenAlex
- W2161506093
- Cited by
- 158
- References
- 70
- Citations by year
- 2026: 6 · 2025: 10 · 2024: 11 · 2023: 15 · 2022: 15 · 2021: 18 · 2020: 12 · 2019: 9 · 2018: 8 · 2017: 14 · 2016: 11 · 2015: 12 · 2014: 9 · 2013: 8
- FWCI
- 5.97
- Type
- journal article
- Language
- en
- Open access
- green
- europepmc.org
- Locations
- American Journal of Physiology-Heart and Circulatory Physiology (publishedVersion)
- Europe PMC (PubMed Central) (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Institutes of Health (UL1TR000117, UL1TR001998)
- National Heart, Lung, and Blood Institute (R01HL098945, R01HL090749)
- National Institute of Environmental Health Sciences (RC1ES018636)
- National Institute of Arthritis and Musculoskeletal and Skin Diseases (R01AR048816, R01AR055246)
- National Center for Advancing Translational Sciences
- Topics
- Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Cardiomyopathy and Myosin Studies
- Life Sciences › Neuroscience › Endocrine and Autonomic Systems › Circadian rhythm and melatonin
- Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Cardiac electrophysiology and arrhythmias
- Keywords
- dilated cardiomyopathy, Bmal1, clock genes, circadian rhythm disruption, cardiac hypertrophy, cardiac remodeling, myosin heavy chain isoforms, titin isoforms, sarcomere structure
- MeSH terms
- Age Factors, Aging, Animals, Cardiomyopathy, Dilated, Gene Expression Regulation, Heart Failure, Mice, Inbred C57BL, Muscle Proteins, Myocardial Contraction, Myocardium, Protein Kinases, RNA, Messenger, Sarcomeres, Stroke Volume, Ultrasonography, Ventricular Function, Left, Hypertrophy, Left Ventricular, Ventricular Pressure, Mice, Knockout, Disease Progression, Ventricular Dysfunction, Left, Myosin Heavy Chains, Mice, ARNTL Transcription Factors, Connectin
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