ArticleScientific reports2015
FFA-ROS-P53-mediated mitochondrial apoptosis contributes to reduction of osteoblastogenesis and bone mass in type 2 diabetes mellitus.
Article in Scientific reports, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed, 43 citations in OpenAlex.
- Integrative bioinformatics and machine learning reveal hub genes and immune signatures bridging type 2 diabetes mellitus, fracture susceptibility, and osteoblast differentiation dysfunction.Mammalian genome : official journal of the International Mammalian Genome Society · 2026Article
- Targeting innate immunity to modulate bone metabolism: a novel strategy for osteoporosis treatment.Frontiers in aging · 2026Review
- Functionalized GelMA-based hydrogels for osteoimmunomodulation and bone regeneration.Frontiers in bioengineering and biotechnology · 2026Review
- CDCP1 allosterically regulates the AMPK α1 subunit to enhance fatty acid oxidation in osteoblasts.Cellular & molecular biology letters · 2025Article
- Dnmt3a-mediated DNA Methylation Regulates P. gingivalis-suppressed Cementoblast Mineralization Partially Via Mitochondria-dependent Apoptosis Pathway.Inflammation · 2025Article
- Integrated Metabolomics and Lipidomics Analysis Reveals the Mechanism Behind the Action of Chiglitazar on the Protection Against Sepsis-Induced Acute Lung Injury.Metabolites · 2025Article
- The multifaceted roles of mitochondria in osteoblasts: from energy production to mitochondrial-derived vesicle secretion.Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research · 2024Review
- Biomaterials Designed to Modulate Reactive Oxygen Species for Enhanced Bone Regeneration in Diabetic Conditions.Journal of functional biomaterials · 2024Review
- Targeting mitochondrial dysfunction using methylene blue or mitoquinone to improve skeletal aging.Aging · 2024Article
- Osteogenesis of bone marrow mesenchymal stem cell in hyperglycemia.Frontiers in endocrinology · 2023Review
- Tocopherol attenuates the oxidative stress of BMSCs by inhibiting ferroptosis through the PI3k/AKT/mTOR pathway.Frontiers in bioengineering and biotechnology · 2022Article
- Glucose Metabolism in Osteoblasts in Healthy and Pathophysiological Conditions.International journal of molecular sciences · 2021Review
- H2S Donor and Bone Metabolism.Frontiers in pharmacology · 2021Review
- Novel Insights and Current Evidence for Mechanisms of Atherosclerosis: Mitochondrial Dynamics as a Potential Therapeutic Target.Frontiers in cell and developmental biology · 2021Review
- Mitochondrial Dysfunction in Chronic Respiratory Diseases: Implications for the Pathogenesis and Potential Therapeutics.Oxidative medicine and cellular longevity · 2021Review
- Targeted Inhibition of LPL/FABP4/CPT1 fatty acid metabolic axis can effectively prevent the progression of nonalcoholic steatohepatitis to liver cancer.International journal of biological sciences · 2021Article
- Therapeutic potentials and modulatory mechanisms of fatty acids in bone.Cell proliferation · 2020Review
- Isopsoralen ameliorates HExperimental and therapeutic medicine · 2019Article
- Stem cell-based bone and dental regeneration: a view of microenvironmental modulation.International journal of oral science · 2019Review
- Inhalation of Hydrogen Attenuates Progression of Chronic Heart Failure via Suppression of Oxidative Stress and P53 Related to Apoptosis Pathway in Rats.Frontiers in physiology · 2018Article
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Authors and funding
4 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
This study evaluated the association between free fatty acid (FFA), ROS generation, mitochondrial dysfunction and bone mineral density (BMD) in type 2 diabetic patients and investigated the molecular mechanism. db/db and high fat (HF)-fed mice were treated by Etomoxir, an inhibitor of CPT1, MitoQ, and PFT-α, an inhibitor of P53. Bone metabolic factors were assessed and BMSCs were isolated and induced to osteogenic differentiation. FFA, lipid peroxidation and mtDNA copy number were correlated with BMD in T2DM patients. Etomoxir, MitoQ and PFT-α significantly inhibited the decrease of BMD and bone breaking strength in db/db and HF-fed mice and suppressed the reduction of BMSCs-differentiated osteoblasts. Etomoxir and MitoQ, but not PFT-α, inhibited the increase of mitochondrial ROS generation in db/db and HF-fed mice and osteoblasts. In addition, Etomoxir, MitoQ and PFT-α significantly inhibited mitochondrial dysfunction in osteoblasts. Moreover, mitochondrial apoptosis was activated in osteoblasts derived from db/db and HF-fed mice, which was inhibited by Etomoxir, MitoQ and PFT-α. Furthermore, mitochondrial accumulation of P53 recruited Bax and initiated molecular events of apoptotic events. These results demonstrated that fatty acid oxidation resulted in ROS generation, activating P53/Bax-mediated mitochondrial apoptosis, leading to reduction of osteogenic differentiation and bone loss in T2DM.
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