Cited by 158Cardiomyopathy and Myosin StudiesCircadian rhythm and melatoninCardiac electrophysiology and arrhythmias

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Development of dilated cardiomyopathy in Bmal1-deficient mice

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Lefta, Mellani, Campbell, Kenneth S., Feng, Han-Zhong, Jin, Jian-Ping, Esser, Karyn A.·2012·American Journal of Physiology-Heart and Circulatory Physiology

DOI 10.1152/ajpheart.00238.2012PMC PMC3423146

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Abstract

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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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.
ORCID: Campbell, Kenneth S.
Jin, Jian-Ping
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
DOI: 10.1152/ajpheart.00238.2012
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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Development of dilated cardiomyopathy in Bmal1-deficient mice

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