Mechanism of RNA-modifying enzyme METTL5 in supporting bone formation elucidated: International research discovers antioxidant regulatory mechanism linked to bone formation defects
An international research group, including Professor Shoichiro Kokabu of the Kyushu Dental University, has elucidated how the RNA-modifying enzyme METTL5 maintains the antioxidant function of osteoblasts to support normal bone formation. METTL5 deficiency leads to reduced OSER1 protein production, causing bone formation defects due to oxidative stress. The study, published in JCI Insight, suggests potential for new therapeutic approaches targeting antioxidant regulation.
📋 Article Processing Timeline
- 📰 Published: June 1, 2026 at 14:00
- 🔍 Collected: June 1, 2026 at 14:27 (27 min after Published)
- 🤖 AI Analyzed: June 1, 2026 at 14:42 (14 min after Collected)
An international research group, including Professor Shoichiro Kokabu of the Department of Biochemistry at Kyushu Dental University, in collaboration with Professor Quan Yuan of West China School of Stomatology, Sichuan University, has revealed that the RNA-modifying enzyme METTL5 protects bone-forming cells from oxidative stress and supports normal bone formation. These findings deepen the understanding of METTL5-related diseases and bone formation defects, potentially leading to the development of new therapies targeting antioxidant regulation. The results were published in the international medical and life sciences journal JCI Insight on May 8, 2026.
Key points of the research:
- METTL5-deficient mice exhibit smaller body size, reduced bone mass, and impaired bone formation.
- METTL5 regulates the production of OSER1 protein to maintain the antioxidant function of osteoblasts.
- METTL5 deficiency reduces the antioxidant capacity of osteoblasts, making them vulnerable to oxidative stress.
- Administration of the antioxidant N-acetylcysteine (NAC) partially improves bone formation defects caused by METTL5 deficiency.
Research content and results:
The research group investigated the role of METTL5 in bone formation. Analysis of METTL5-deficient mice showed smaller body size and reduced bone mass compared to normal mice. Further investigation revealed that while bone-resorbing cells remained largely unchanged, the function of bone-forming osteoblasts was weakened. This indicated that the loss of METTL5 primarily reduces the 'bone-building' capacity. Furthermore, METTL5 deficiency led to insufficient production of the OSER1 protein, reducing the cells' ability to protect themselves against oxidative stress. Finally, administration of the antioxidant NAC partially restored the antioxidant function and bone-forming capacity of the cells. These results demonstrate that METTL5 maintains normal bone formation by supporting OSER1 production, thereby protecting osteoblasts from oxidative stress.
Key points of the research:
- METTL5-deficient mice exhibit smaller body size, reduced bone mass, and impaired bone formation.
- METTL5 regulates the production of OSER1 protein to maintain the antioxidant function of osteoblasts.
- METTL5 deficiency reduces the antioxidant capacity of osteoblasts, making them vulnerable to oxidative stress.
- Administration of the antioxidant N-acetylcysteine (NAC) partially improves bone formation defects caused by METTL5 deficiency.
Research content and results:
The research group investigated the role of METTL5 in bone formation. Analysis of METTL5-deficient mice showed smaller body size and reduced bone mass compared to normal mice. Further investigation revealed that while bone-resorbing cells remained largely unchanged, the function of bone-forming osteoblasts was weakened. This indicated that the loss of METTL5 primarily reduces the 'bone-building' capacity. Furthermore, METTL5 deficiency led to insufficient production of the OSER1 protein, reducing the cells' ability to protect themselves against oxidative stress. Finally, administration of the antioxidant NAC partially restored the antioxidant function and bone-forming capacity of the cells. These results demonstrate that METTL5 maintains normal bone formation by supporting OSER1 production, thereby protecting osteoblasts from oxidative stress.
FAQ
How does this research impact medical practices in Taiwan?
By advancing the understanding of bone disease pathology, it contributes to the future development of diagnostic techniques and novel therapies using antioxidant regulation.