ArticleAmerican journal of physiology. Heart and circulatory physiology2015
Cardiomyocyte-specific Bmal1 deletion in mice triggers diastolic dysfunction, extracellular matrix response, and impaired resolution of inflammation.
Article in American journal of physiology. Heart and circulatory physiology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 81 papers, 1 of them a synthesis that pooled it.
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Who cites it
81 citing papers in PubMed, 1 synthesis or guideline pooled it, 106 citations in OpenAlex.
- A Review of CXCL1 in Cardiac Fibrosis.Frontiers in cardiovascular medicine · 2021Pooled it
- Circadian mechanisms in heart failure: Cell-specific regulation and chrono-medicine.Cell insight · 2026Review
- Type 1 diabetes differentially disrupts right and left ventricular daily rhythms.Function (Oxford, England) · 2026Article
- Discovery of circadian clock activators with anti-obesity efficacy via suppression of adipocyte development and hypertrophy.Molecular therapy : the journal of the American Society of Gene Therapy · 2026Article
- Circadian regulation of cardiovascular function: from physiology to clinical implications.Genome medicine · 2026Review
- Unlocking the potential of circadian biology for cardiovascular health.Physiological reviews · 2026Review
- BMAL1 attenuates myocardial infarction-induced fibrosis via suppressing p-SMAD3/SMAD3 in TGF-β1 pathway.Biochemistry and biophysics reports · 2026Article
- The Cardiac Circadian Clock Regulates Rhythms in Peripheral Tissues via Fibulin 5.Comprehensive physiology · 2026Article
- Timing matters: circadian rhythm disruption in alcohol-associated peripheral organ pathophysiology.Function (Oxford, England) · 2026Review
- Novel circadian clock activators display anti-obesity efficacy via suppression of adipocyte development and hypertrophy.bioRxiv : the preprint server for biology · 2026Article
- Circadian control of immune homeostasis in cardiovascular health and disease.Frontiers in immunology · 2026Review
- Deletion of Circadian Rhythms Gene BMAL1 Impairs the Intestinal Epithelial Barrier and Exacerbates Intestinal Inflammation by Inducing Pyroptosis.Mediators of inflammation · 2026Article
- Circadian clock genes and insomnia: molecular mechanisms and therapeutic implications.Annals of medicine · 2025Review
- Twenty-Four Hour Rhythms in Cardiovascular Physiology.Acta physiologica (Oxford, England) · 2025Review
- Research Progress of BMAL1 in Heart Failure.Journal of the American Heart Association · 2025Review
- Time to Reset: The Interplay Between Circadian Rhythms and Redox Homeostasis in Skeletal Muscle Ageing and Systemic Health.Antioxidants (Basel, Switzerland) · 2025Review
- Identification of metabolic pathways and serum biomarkers in diabetic cardiomyopathy using untargeted metabolomics.Scientific reports · 2025Article
- BMAL1 in Ischemic Heart Disease: A Narrative Review from Molecular Clock to Myocardial Pathology.International journal of molecular sciences · 2025Review
- Article
- Circadian biology of cardiac aging.Journal of molecular and cellular cardiology · 2025Review
21 more citing papers are in PubMed but not listed here.
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
The mammalian circadian clock consists of multiple transcriptional regulators that coordinate biological processes in a time-of-day-dependent manner. Cardiomyocyte-specific deletion of the circadian clock component, Bmal1 (aryl hydrocarbon receptor nuclear translocator-like protein 1), leads to age-dependent dilated cardiomyopathy and decreased lifespan in mice. We investigated whether cardiomyocyte-specific Bmal1 knockout (CBK) mice display early alterations in cardiac diastolic function, extracellular matrix (ECM) remodeling, and inflammation modulators by investigating CBK mice and littermate controls at 8 and 28 wk of age (i.e., prior to overt systolic dysfunction). Left ventricles of CBK mice exhibited (P < 0.05): 1) progressive abnormal diastolic septal annular wall motion and reduced pulmonary venous flow only at 28 wk of age; 2) progressive worsening of fibrosis in the interstitial and endocardial regions from 8 to 28 wk of age; 3) increased (>1.5 fold) expression of collagen I and III, as well as the matrix metalloproteinases MMP-9, MMP-13, and MMP-14 at 28 wk of age; 4) increased transcript levels of neutrophil chemotaxis and leukocyte migration genes (Ccl2, Ccl8, Cxcl2, Cxcl1, Cxcr2, Il1β) with no change in Il-10 and Il-13 genes expression; and 5) decreased levels of 5-LOX, HO-1 and COX-2, enzymes indicating impaired resolution of inflammation. In conclusion, genetic disruption of the cardiomyocyte circadian clock results in diastolic dysfunction, adverse ECM remodeling, and proinflammatory gene expression profiles in the mouse heart, indicating signs of early cardiac aging in CBK mice.
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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.