Hydrogen Gas Prevents Bone Loss by Blocking Bone-Destroying Cells
- Authors
- Yong Liu, Wei Wang, Yong Zeng, Hui Zeng
- Journal
- Experimental and Therapeutic Medicine
- Year
- 2023
- DOI
- 10.3892/etm.2023.12135
- Study Type
- Mouse
- Outcome
- Positive
- Peer Reviewed
- Yes
- Country
- China
- Health Condition
- Osteoporosis
- Body System
- Skeletal
TL;DR
Hydrogen gas, produced by magnesium alloys used in bone healing, can help in fracture repair by blocking the development of bone-resorbing cells through specific genetic changes.
Key Finding
Hydrogen gas inhibits the formation of bone-resorbing cells by activating protective genes and suppressing bone-breakdown genes through multiple cellular signaling pathways.
Summary
Researchers studied how hydrogen gas affects bone cells in mice, specifically cells that break down bone (osteoclasts). Using genetic analysis, they found that hydrogen gas changes which genes are active in these cells, turning on protective genes and turning off genes that promote bone breakdown. This suggests hydrogen gas could help bones heal better and may be useful for treating conditions like osteoporosis where bones become weak.
Practical Takeaway
This is an early-stage mouse study that identifies potential molecular mechanisms for how hydrogen might support bone health. While the findings are promising for future development of hydrogen-based bone therapies, this research does not yet demonstrate effects in humans, and much more work is needed before any clinical applications can be considered.
Abstract
Hydrogen (H2) is a major biodegradation product of implanted magnesium (Mg) alloys that are commonly used in the healing of bone fractures. Our earlier study showed that H2 can inhibit mouse bone marrow mononuclear cell (BMMC) osteoclastogenesis during the differentiation of these cells into osteoclasts, thereby facilitating fracture healing. However, the way by which H2 inhibits osteoclastogenesis remains to be elucidated. The present study used RNA-sequencing to study the transcriptome of H2-exposed BMMCs in an osteoclast-induced environment and identified the target genes and signaling pathways through which H2 exerts its biological effects. Several upregulated genes were identified: Fos, Dusp1, Cxcl1, Reln, Itga2b, Plin2, Lif, Thbs1, Vegfa and Gadd45a. Several downregulated genes were also revealed: Hspa1b, Gm4951, F830016B08Rik, Fads2, Hspa1a, Slc27a6, Cacna1b, Scd2, Lama3 and Col4a5. These differentially expressed genes were mainly involved in osteoclast differentiation cascades, as well as PI3K-AKT, Forkhead box O (FoxO), MAPK, peroxisome proliferator-activated receptor (PPAR), TNF, TGF-β, JAK-STAT, RAS, VEGF, hypoxia-inducible factor (HIF-1) and AMPK signaling pathways. In summary, the present study revealed the key genes and signaling pathways involved in the H2-mediated inhibition of osteoclastogenesis, thereby providing a theoretical basis for the significance of H2 and an experimental basis for the application of Mg alloys in the treatment of osteoporosis.