ArticleMolecular biology reports2018
BMAL1 regulates balance of osteogenic-osteoclastic function of bone marrow mesenchymal stem cells in type 2 diabetes mellitus through the NF-κB pathway.
Article in Molecular biology reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 24 citations in OpenAlex.
- Ion sequential therapy aligned with pathological changes enhances cardiac function after myocardial infarction.Cell reports. Medicine · 2026Article
- HIF-1α and BMAL1 in bone regeneration: crosstalk between hypoxia response and circadian rhythm.Bone research · 2026Review
- Tuned by time: the role of circadian rhythms in metabolic energy sensing and chronotherapy.Annals of medicine · 2025Review
- Signaling pathway mechanisms of circadian clock gene Bmal1 regulating bone and cartilage metabolism: a review.Bone research · 2025Review
- Exploring the association between circadian rhythms and osteoporosis: new diagnostic and therapeutic targets identified via machine learning.Frontiers in molecular biosciences · 2025Article
- The Circadian Clock Gene Bmal1 Regulates Microglial Pyroptosis After Spinal Cord Injury via NF-κB/MMP9.CNS neuroscience & therapeutics · 2024Article
- Effect of Circadian Rhythm Disturbance on the Human Musculoskeletal System and the Importance of Nutritional Strategies.Nutrients · 2023Review
- Clock genes are expressed in cementum and regulate the proliferation and mineralization of cementoblasts.In vitro cellular & developmental biology. Animal · 2023Article
- Cholesterol inhibits autophagy in RANKL-induced osteoclast differentiation through activating the PI3K/AKT/mTOR signaling pathway.Molecular biology reports · 2022Article
- Co-regulation of circadian clock genes and microRNAs in bone metabolism.Journal of Zhejiang University. Science. B · 2022Review
- The role of circadian rhythm in osteoporosis; a review.Frontiers in cell and developmental biology · 2022Review
- Challenges to Improve Bone Healing Under Diabetic Conditions.Frontiers in endocrinology · 2022Review
- Critical Roles of the Circadian Transcription FactorFrontiers in endocrinology · 2022Review
- Chronic Circadian Rhythm Disturbance Accelerates Knee Cartilage Degeneration in Rats Accompanied by the Activation of the Canonical Wnt/β-Catenin Signaling Pathway.Frontiers in pharmacology · 2021Article
- Targeting Stem Cells in Chronic Inflammatory Diseases.Advances in experimental medicine and biology · 2021Review
- Gut microbiota: closely tied to the regulation of circadian clock in the development of type 2 diabetes mellitus.Chinese medical journal · 2020Review
- Rev-erbα Negatively Regulates Osteoclast and Osteoblast Differentiation through p38 MAPK Signaling Pathway.Molecules and cells · 2020Article
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
In bone marrow mesenchymal stem cell (BMSCs), type 2 diabetes mellitus (T2DM) induces metabolic and functional disorders, leading to imbalanced bone resorption and formation and bone loss. Brain and muscle ARNT-like protein 1 (BMAL1) is involved in regulating T2DM-related suppression of BMSCs osteogenesis and bone formation. However, the relationship between BMAL1 and bone remodelling, especially bone resorption in T2DM, is unclear. We investigated the antergic role played by BMAL1 in T2DM-prompted imbalance in BMSCs osteogenic-osteoclastic function. BMAL1 was inhibited and the receptor activator of nuclear factor-κB ligand/osteoprotegerin (RANKL/OPG) ratio was increased in diabetic BMSCs. Inhibitor κB (IκB) expression was decreased, whereas phosphorylated-p65 (p-p65), caspase-3, and p-IκB expression were increased in diabetic BMSCs. BMAL1 overexpression recovered the osteogenesis ability and suppressed osteoclastic induction capability of BMSCs to improve bone metabolism and function, which was partially due to NF-κB pathway activity inhibition. Our results provide evidence about the role of BMAL1 in T2DM-prompted BMSCs differentiation dysfunction, i.e. partially decreasing NF-κB pathway expression. In T2DM, it might be possible to use overexpressed BMAL1 to re-establish the homeostasis of bone metabolism.
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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.