ArticleJournal of the American Heart Association2022
Postnatal Deletion of Bmal1 in Cardiomyocyte Promotes Pressure Overload Induced Cardiac Remodeling in Mice.
Article in Journal of the American Heart Association, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 24 citations in OpenAlex.
- BMAL1 attenuates myocardial infarction-induced fibrosis via suppressing p-SMAD3/SMAD3 in TGF-β1 pathway.Biochemistry and biophysics reports · 2026Article
- Impact of E-Cigarette Use on Circadian Proteins and Cardiovascular Risk Markers.Journal of cardiovascular translational research · 2026Article
- Dual roles of circadian clock proteins in development and adult homeostasis.Npj biological timing and sleep · 2026Review
- 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
- Time to Reset: The Interplay Between Circadian Rhythms and Redox Homeostasis in Skeletal Muscle Ageing and Systemic Health.Antioxidants (Basel, Switzerland) · 2025Review
- Aerobic Exercise and PI3K Inhibitor Ameliorate Obesity Cardiomyopathy by Alleviating Pyroptosis in Middle-Aged Mice.International journal of molecular sciences · 2025Article
- Article
- Circadian biology of cardiac aging.Journal of molecular and cellular cardiology · 2025Review
- Single-cell transcriptomic profiling of heart reveals ANGPTL4 linking fibroblasts and angiogenesis in heart failure with preserved ejection fraction.Journal of advanced research · 2025Article
- Exosomes From Human Umbilical Cord Stem Cells Suppress Macrophage-to-myofibroblast Transition, Alleviating Renal Fibrosis.Inflammation · 2024Article
- Circadian rhythms in cardiovascular (dys)function: approaches for future therapeutics.NPJ cardiovascular health · 2024Review
- Article
- Disturbance of suprachiasmatic nucleus function improves cardiac repair after myocardial infarction by IGF2-mediated macrophage transition.Acta pharmacologica Sinica · 2023Article
- Voluntary Wheel Running Exercise Does Not Attenuate Circadian and Cardiac Dysfunction Caused by Conditional Deletion ofJournal of biological rhythms · 2023Article
- Long-Term Transcriptomic Changes and Cardiomyocyte Hyperpolyploidy after Lactose Intolerance in Neonatal Rats.International journal of molecular sciences · 2023Article
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background Mice with cardiomyocyte-specific deletion of Bmal1, a core clock gene, had spontaneous abnormal cardiac metabolism, dilated cardiomyopathy, and shortened lifespan. However, the role of cardiomyocyte Bmal1 in pressure overload induced cardiac remodeling is unknown. Here we aimed to understand the contribution of cardiomyocyte Bmal1 to cardiac remodeling in response to pressure overload induced by transverse aortic constriction or chronic angiotensin Ⅱ (AngⅡ) infusion. Methods and Results By generating a tamoxifen-inducible cardiomyocyte-specific Bmal1 knockout mouse line (cKO) and challenging the mice with transverse aortic constriction or AngⅡ, we found that compared to littermate controls, the cKO mice displayed remarkably increased cardiac hypertrophy and augmented fibrosis both after transverse aortic constriction and AngⅡ induction, as assessed by echocardiographic, gravimetric, histologic, and molecular analyses. Mechanistically, RNA-sequencing analysis of the heart after transverse aortic constriction exposure revealed that the PI3K/AKT signaling pathway was significantly activated in the cKOs. Consistent with the in vivo findings, in vitro study showed that knockdown of Bmal1 in cardiomyocytes significantly promoted phenylephrine-induced cardiomyocyte hypertrophy and triggered fibroblast-to-myofibroblast differentiation, while inhibition of AKT remarkedly reversed the pro-hypertrophy and pro-fibrosis effects of Bmal1 knocking down. Conclusions These results suggest that postnatal deletion of Bmal1 in cardiomyocytes may promote pressure overload-induced cardiac remodeling. Moreover, we identified PI3K/AKT signaling pathway as the potential mechanistic ties between Bmal1 and cardiac remodeling.
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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.