ArticleMolecular medicine reports2020
Excessive production of mitochondrion‑derived reactive oxygen species induced by titanium ions leads to autophagic cell death of osteoblasts via the SIRT3/SOD2 pathway.
Article in Molecular medicine reports, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 24 citations in OpenAlex.
- Mitochondrial antioxidant enzyme (SOD2) at the crossroads of redox signaling and cancer progression.Free radical research · 2026Review
- The impact of biocorrosion and titanium ions release on peri-implantitis.Clinical oral investigations · 2025Review
- SIRT3: A Potential Target of Different Types of Osteoporosis.Cell biochemistry and biophysics · 2024Review
- Identification and analysis of mitochondria-related central genes in steroid-induced osteonecrosis of the femoral head, along with drug prediction.Frontiers in endocrinology · 2024Article
- Primary Hypothyroidism and Alzheimer's Disease: A Tale of Two.Cellular and molecular neurobiology · 2023Review
- The role of mitochondria in the peri-implant microenvironment.Experimental physiology · 2023Review
- The Potential of Natural Compounds Regulating Autophagy in the Treatment of Osteoporosis.Journal of inflammation research · 2023Review
- Role of SIRT3 in bone homeostasis and its application in preventing and treating bone diseases.Frontiers in pharmacology · 2023Review
- Wenshen Yangxue decoction promotes follicular development in aged female mice stimulation of the silent information regulator 3/forkhead transcription factor O1 3a pathway.Journal of traditional Chinese medicine = Chung i tsa chih ying wen pan · 2022Article
- Osteoblast lineage Sod2 deficiency leads to an osteoporosis-like phenotype in mice.Disease models & mechanisms · 2022Article
- Reversal of Doxorubicin-Induced Bone Loss and Mineralization by Supplementation of Resveratrol and MitoTEMPO in the Early Development ofNutrients · 2022Article
- The Role of SIRT3 in the Osteoporosis.Frontiers in endocrinology · 2022Review
- The Effect of SIRT3/Ac-SOD2 Mediated Oxidative Stress and HCN1 Channel Activity on Anesthesia/Surgery Induced Anxiety-Like Behavior in Mice.Frontiers in medicine · 2022Article
- A study of hydrophobins-modified menaquinone-7 on osteoblastic cells differentiation.Molecular and cellular biochemistry · 2021Article
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The incidence of peri-implant bone loss is high, and is a difficult condition to treat. Previous studies have shown that titanium (Ti) ions released from implants can lead to osteoblast cell damage, but the specific mechanisms have not been elucidated. The present study established a Ti ion damage osteoblast cell model. The levels of mitochondrion‑derived reactive oxygen species (mROS) and autophagy, cell viability and the sirtuin 3 (SIRT3)/superoxide dismutase 2 (SOD2) pathway were examined in this model. It was found that Ti ions decreased osteoblast viability. Moreover, with increased Ti ion concentration, the expression levels of microtubule associated protein 1 light chain 3α (LC3) progressively increased, P62 decreased, autophagic flow increased and mROS levels increased. After the addition of an autophagy inhibitor Bafilomycin A1 and Mito‑TEMPO, a mitochondrial antioxidant, the production of mROS was inhibited, the level of autophagy was decreased and cell activity was improved. In addition, with increased Ti ion concentration, the activity of SOD2 decreased, the acetylation level of SOD2 increased, the SIRT3 mRNA and protein expression levels decreased, and the activity of SIRT3 was significantly decreased. Furthermore, it was demonstrated that SIRT3 overexpression reduced the acetylation of SOD2 and increased the activity of SOD2, as well as reducing the production of mROS and the expression level of LC3, thus increasing cell viability. Therefore, the present results suggested that excessive production of mROS induced by Ti ions led to autophagic cell death of osteoblasts, which is dependent on the SIRT3/SOD2 pathway.
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