ArticleAmerican journal of physiology. Heart and circulatory physiology2012
Development of dilated cardiomyopathy in Bmal1-deficient mice.
Article in American journal of physiology. Heart and circulatory physiology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 99 papers, 1 of them a synthesis that pooled it.
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Who cites it
99 citing papers in PubMed, 1 synthesis or guideline pooled it, 157 citations in OpenAlex.
- Circadian rhythm disruption in cardiovascular disease: a systematic review and meta-analysis of mechanistic evidence from animal models.BMC medicine · 2026Pooled it
- Expression of HO1 and PER2 can predict the incidence of delirium in trauma patients with concomitant brain injury.Scientific reports · 2021Trial
- Circadian mechanisms in heart failure: Cell-specific regulation and chrono-medicine.Cell insight · 2026Review
- BMAL1 in cardiovascular diseases: Molecular mechanisms, circadian regulation and translational perspectives (Review).Molecular medicine reports · 2026Review
- A newly developed circadian imbalance index (CII) and risk of cardiovascular-kidney-metabolic disease in the UK biobank.European journal of epidemiology · 2026Article
- Location and aetiology are determinants of fibroblast activation and heterogeneity in the failing human heart.Genome medicine · 2025Article
- Neurobiology of the circadian clock and its role in cardiovascular disease: Mechanisms, biomarkers, and chronotherapy.Neurobiology of sleep and circadian rhythms · 2025Review
- Research Progress of BMAL1 in Heart Failure.Journal of the American Heart Association · 2025Review
- Article
- Interaction between clock genes, melatonin and cardiovascular outcomes from ICU patients.Intensive care medicine experimental · 2025Article
- The chronobiology of human heart failure: clinical implications and therapeutic opportunities.Heart failure reviews · 2025Review
- Circadian Rhythm and Muscle Function.Advances in experimental medicine and biology · 2025Review
- Role of circadian transcription factor REV-ERB in cardiovascular diseases: a review.Frontiers in cardiovascular medicine · 2025Review
- Targeted Bmal1 restoration in muscle prolongs lifespan with systemic health effects in aging model.JCI insight · 2024Article
- Circadian rhythms in cardiovascular (dys)function: approaches for future therapeutics.NPJ cardiovascular health · 2024Review
- Circadian Regulation of Cardiac Arrhythmias and Electrophysiology.Circulation research · 2024Review
- Circadian Influences on Myocardial Ischemia-Reperfusion Injury and Heart Failure.Circulation research · 2024Review
- Cardiac Timeless Trans-Organically Regulated by miR-276 in Adipose Tissue Modulates Cardiac Function.Function (Oxford, England) · 2024Article
- The interplay between sex, time of day, fasting status, and their impact on cardiac mitochondrial structure, function, and dynamics.Scientific reports · 2023Article
- The Cardiac Circadian Clock: Implications for Cardiovascular Disease and its Treatment.JACC. Basic to translational science · 2023Review
39 more citing papers are in PubMed but not listed here.
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Authors and funding
5 authors at 2 institutions in 1 country.
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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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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.