ArticleInternational journal of biological sciences2017
Sirtuin 3 is required for osteogenic differentiation through maintenance of PGC-1ɑ-SOD2-mediated regulation of mitochondrial function.
Article in International journal of biological sciences, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 56 papers, 1 of them a synthesis that pooled it.
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Who cites it
56 citing papers in PubMed, 1 synthesis or guideline pooled it, 75 citations in OpenAlex.
- Effects of advanced glycation end products (AGEs) on the differentiation potential of primary stem cells: a systematic review.Stem cell research & therapy · 2023Pooled it
- Bone organoids and mitochondrial reprogramming.Journal of orthopaedic translation · 2026Review
- PFKM acts as a metabolic switch initiating donut-shaped mitochondrial remodeling to promote osteogenesis.International journal of oral science · 2026Article
- IDH2 lactylation regulates mitochondrial dysfunction injury induced by myocardial ischemia‑reperfusion via the AMPK signaling pathway.International journal of molecular medicine · 2026Article
- miR-1290 serves as a potential biomarker for osteoporotic fracture and regulates osteoblast function by targeting KDM5A.Journal of orthopaedic surgery and research · 2026Article
- Fermented and Unfermented Rooibos (Antioxidants (Basel, Switzerland) · 2026Article
- Mitigating mitochondrial dysfunction: a novel strategy for Chinese botanical drugs against osteoporosis.Frontiers in pharmacology · 2026Review
- CAF-derived BHB modulates FXR1-Kbhb and NK-cell lipid metabolism in osteosarcoma.International journal of biological sciences · 2026Article
- PGC-1α: key regulator of mitochondrial biogenesis and cellular differentiation in metabolic and regenerative tissues.Cell & bioscience · 2025Review
- Understanding the molecular basis of mesenchymal stem cell stemness: implications for clinical applications.Cell death & disease · 2025Review
- Sirt3 Rescues Porphyromonas gingivalis-Impaired Cementogenesis via SOD2 Deacetylation.Cell proliferation · 2025Article
- NMN improves cardiac function in SIRT3 knockout mice via the SIRT1/PGC-1α pathway.Scientific reports · 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
- Mitochondrial dysfunction and aging: multidimensional mechanisms and therapeutic strategies.Biogerontology · 2025Review
- SENP3 alleviates osteoporosis via promoting SIRT3 transcription through the increase of DLX2 stability via SUMO2/3.Cell biology and toxicology · 2025Article
- Role of sirtuins in obesity and osteoporosis: molecular mechanisms and therapeutic targets.Cell communication and signaling : CCS · 2025Review
- The Critical Role of Autophagy in the Pathogenesis of Diabetic Osteoporosis: Mechanisms and Therapeutic Measures.Drug design, development and therapy · 2025Review
- Significant Interaction between Melatonin and Titanium Bone Implants: Available Evidence and Future Research Directions.Current pharmaceutical biotechnology · 2025Review
- Sirtuin 3-activated superoxide dismutase 2 mediates fluoride-induced osteoblastic differentiation in vitro and in vivo by down-regulating reactive oxygen species.Archives of toxicology · 2024Article
- The Emerging Role of the Mitochondrial Respiratory Chain in Skeletal Aging.Aging and disease · 2024Review
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Osteogenic differentiation is crucial for the maintenance of bone homeostasis. Sirtuin 3 (SIRT3), a member of sirtuins family, functions as a critical deacetylase that regulates many key proteins. In the current study, we aimed to clarify the role of SIRT3 in osteogenic differentiation and the possible mechanisms, using mouse pre-osteoblastic MC3T3-E1 cells. Expression of SIRT3 was substantially increased in differentiated MC3T3-E1 cells. Knock down of SIRT3 significantly decreased alkaline phosphatase (ALP) staining, and mRNA expression of runt-related transcription factor 2 (Runx2) and collagen type I ɑ 1 (Col1ɑ1), and osteocalcin in differentiated MC3T3-E1 cells. Overexpression of wild type but not mutant SIRT3 could reverse SIRT3 knockdown-resulted decrease of ALP staining. Complex I, II, III, IV, and V activities, oxygen consumption and mitochondrial membrane potential were significantly decreased by SIRT3 knockdown. Moreover, SIRT3 knockdown reduced mitochondrial density, increased mitochondrial size and decreased the expression of NRF1 and TFAM. Knock down of SIRT3 decreased mRNA and protein expression of SOD2 and increased ROS level. Overexpression of SOD2 significantly suppressed SIRT3 knockdown-induced decrease of mitochondrial function and osteogenic differentiation. SIRT3 knockdown resulted in a significant decrease of PGC-1ɑ protein expression but not mRNA expression. Overexpression of wild type but not mutant SIRT3 could reverse SIRT3 knockdown-resulted decrease of PGC-1ɑ protein expression. Moreover, we detected a direct interaction between SIRT3 and PGC-1ɑ and SIRT3 knockdown reduced SIRT3 and PGC-1ɑ interaction, resulting in a reduction of PGC-1ɑ protein stability and PGC-1ɑ-binding in the promoters of SOD2. Overexpression of PGC-1ɑ blocked SIRT3 knockdown-induced decrease of SOD2 expression, increase of ROS level, and decrease of mitochondrial function and biogenesis, leading to improvement of osteogenesis. Overall, the data provide a better understanding of the role of SIRT3 in osteogenic differentiation.
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