ArticleBone2016
Deficiency of circadian clock protein BMAL1 in mice results in a low bone mass phenotype.
Article in Bone, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 86 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
86 citing papers in PubMed, 124 citations in OpenAlex.
- The Circadian-Melatonin Axis in Bone Remodeling: Receptor-Dependent Signaling, Receptor-Independent Actions, and Translational Constraints.Biomolecules · 2026Review
- Circadian rhythm: The hidden "puppet master" behind musculoskeletal disorders.Journal of orthopaedic translation · 2026Review
- Modeling the Clockwork of Bone: A Narrative Review of Experimental Approaches to Circadian Rhythm in Bone Metabolism.International journal of molecular sciences · 2026Review
- A Circadian Trough in Glucocorticoid Signaling Is Essential for Bone Health in Mice.Aging cell · 2026Article
- HIF-1α and BMAL1 in bone regeneration: crosstalk between hypoxia response and circadian rhythm.Bone research · 2026Review
- Nutritional adaptation to circadian misalignment: implications for musculoskeletal health in modern lifestyles.Frontiers in nutrition · 2026Review
- Chronobiology of fracture repair: local molecular clocks, rhythm protection, and time-anchored translation.Frontiers in endocrinology · 2026Review
- Dual roles of circadian clock proteins in development and adult homeostasis.Npj biological timing and sleep · 2026Review
- Age-dependent association between obstructive sleep apnea and self-reported history of fractures: a community-based study.BMC public health · 2025Article
- Review
- Shaking culture attenuates circadian rhythms in induced pluripotent stem cells during osteogenic differentiation through the TEAD-Fbxl3-CRY axis.Cell death discovery · 2025Article
- Rhythms in Remodeling: Posttranslational Regulation of Bone by the Circadian Clock.Biomedicines · 2025Review
- Signaling pathway mechanisms of circadian clock gene Bmal1 regulating bone and cartilage metabolism: a review.Bone research · 2025Review
- Detection of Insertion/Deletions (InDel) Within Five Clock Genes and Their Associations with Growth Traits in Four Chinese Sheep Breeds.Veterinary sciences · 2025Article
- Epigenetic Mechanisms in the Transcriptional Regulation of Circadian Rhythm in Mammals.Biology · 2025Review
- Differential response of neurons to autophagy modulation in Huntington's disease.Autophagy reports · 2025Article
- Ferroptosis and bone metabolic diseases: the dual regulatory role of the Nrf2/HO-1 signaling axis.Frontiers in cell and developmental biology · 2025Review
- Chronotherapy and intervertebral disc degeneration: understanding the role of circadian rhythm in degenerative processes.Frontiers in cell and developmental biology · 2025Review
- Significant Interaction between Melatonin and Titanium Bone Implants: Available Evidence and Future Research Directions.Current pharmaceutical biotechnology · 2025Review
- Skeletal Phenotyping of Period-1-Deficient Melatonin-Proficient Mice.Journal of pineal research · 2024Article
26 more citing papers are in PubMed but not listed here.
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
The circadian clock is an endogenous time keeping system that controls the physiology and behavior of many organisms. The transcription factor Brain and Muscle ARNT-like Protein 1 (BMAL1) is a component of the circadian clock and necessary for clock function. Bmal1(-/-) mice display accelerated aging and many accompanying age associated pathologies. Here, we report that mice deficient for BMAL1 have a low bone mass phenotype that is absent at birth and progressively worsens over their lifespan. Accelerated aging of these mice is associated with the formation of bony bridges occurring across the metaphysis to the epiphysis, resulting in shorter long bones. Using micro-computed tomography we show that Bmal1(-/-) mice have reductions in cortical and trabecular bone volume and other micro-structural parameters and a lower bone mineral density. Histology shows a deficiency of BMAL1 results in a reduced number of active osteoblasts and osteocytes in vivo. Isolation of bone marrow derived mesenchymal stem cells from Bmal1(-/-) mice demonstrate a reduced ability to differentiate into osteoblasts in vitro, which likely explains the observed reductions in osteoblasts and osteocytes, and may contribute to the observed osteopenia. Our data support the role of the circadian clock in the regulation of bone homeostasis and shows that BMAL1 deficiency results in a low bone mass phenotype.
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What OpenQuestion holds
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.