ArticleThe Journal of biological chemistry2018
Active mitochondria support osteogenic differentiation by stimulating β-catenin acetylation.
Article in The Journal of biological chemistry, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 101 papers.
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Who cites it
101 citing papers in PubMed, 176 citations in OpenAlex.
- New insights into the ACLY-mediated metabolic and epigenetic interplay in macrophages.Journal of enzyme inhibition and medicinal chemistry · 2026Review
- The Role of Glucose Metabolic Reprogramming in Exercise-Attenuated Osteoporosis: a Narrative Review.Sports medicine - open · 2026Review
- Mechano-metabolic axis involves mitochondrial responses via BMP/Smad regulatory effect on cyclophilin D.Bone research · 2026Article
- Immunometabolic Modulation of the Bone Marrow Niche by Bioactive Materials to Rescue Impaired Fracture Healing.Stem cell reviews and reports · 2026Review
- Targeting NSignal transduction and targeted therapy · 2026Article
- Mitochondrial geneTranslational cancer research · 2026Article
- Nutritional Interventions to Optimize Orthobiologic Therapy Quality in Type 2 Diabetes Mellitus: Molecular Mechanisms and Clinical Framework: A Narrative Review.International journal of molecular sciences · 2026Review
- Identification of a Novel Mitochondrial-Related Gene Signature for BMSCs in Osteoporosis Combining Single-Cell and Bulk Transcriptome Data.Biochemical genetics · 2026Article
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- Osteocytic Lipocalin-2 regulates bone formation locally through iron-dependent ferroptosis and Wnt suppression.Cell death discovery · 2026Article
- OTUD1 delays wound healing by regulating endothelial function and angiogenesis in diabetic mice.Journal of advanced research · 2026Article
- Anoctamin 5 mutation leads to abnormal bone homeostasis of GDD by regulating AMPK-dependent glucose metabolism.Frontiers in endocrinology · 2026Article
- Mitochondrial dysfunction in mesenchymal stem cells impairs osteogenesis in radiation-induced bone injury via CaCell death & disease · 2025Article
- SHLP2 restores pre-osteoblastic cells against oxidative stress-induced inflammaging.Scientific reports · 2025Article
- Histone H3K27 acetylation mediated by KAT8 maintains antiviral trained immunity in shrimp induced by inactivated white spot syndrome virus.Communications biology · 2025Article
- An emerging role of mitochondrial quality control in bone metabolism: from molecular mechanisms to targeted therapeutic interventions.Cellular and molecular life sciences : CMLS · 2025Review
- Mechanisms of Ellagic Acid (EA)-Mediated Osteogenic Differentiation of Human Dental Pulp-Derived Stem Cells.ACS omega · 2025Article
- Metabolic Rewiring and Post-Translational Modifications: Unlocking the Mechanisms of Bone Turnover in Osteoporosis.Aging and disease · 2025Review
- Focal Adhesion Kinase Alleviates Simulated Microgravity-Induced Inhibition of Osteoblast Differentiation by Activating Transcriptional Wnt/β-Catenin-BMP2-COL1 and Metabolic SIRT1-PGC-1α-CPT1A Pathways.International journal of molecular sciences · 2025Article
41 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.
Funding
Abstract
Bone marrow stromal (a.k.a. mesenchymal stem) cells (BMSCs) can differentiate into osteoblasts (OBs), adipocytes, or chondrocytes. As BMSCs undergo OB differentiation, they up-regulate mitochondrial oxidative phosphorylation (OxPhos). Here, we investigated the mechanism(s) connecting mitochondrial OxPhos to OB differentiation. First, we found that treating BMSC-like C3H10T1/2 cells with an OxPhos inhibitor reduces their osteogenic potential. Interestingly, ATP levels were not reduced, as glycolysis compensated for the decreased OxPhos. Thus, mitochondria support OB differentiation not only by supplying ATP, but also by other mechanisms. To uncover these mechanisms, we stimulated OxPhos in C3H10T1/2 cells by replacing media glucose with galactose and observed that this substitution increases both OxPhos and osteogenesis even in the absence of osteoinducers. β-Catenin, an important signaling pathway in osteogenesis, was found to be responsive to OxPhos stimulation. β-Catenin activity is maintained by acetylation, and mitochondria generate the acetyl donor acetyl-CoA, which upon entering the Krebs cycle is converted to citrate capable of exiting mitochondria. Cytosolic citrate is converted back to acetyl-CoA by ATP citrate lyase (ACLY). We found that inhibiting ACLY with SB204990 (SB) reverses the galactose-induced β-catenin activity and OB differentiation. This suggested that acetylation is involved in β-catenin activation after forced OxPhos stimulation, and using immunoprecipitation, we indeed detected SB-sensitive β-catenin acetylation. Both β-catenin acetylation and activity increased during osteoinduction coincident with OxPhos activation. These findings suggest that active mitochondria support OB differentiation by promoting β-catenin acetylation and thus activity.
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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.