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Sialin-STAT3 axis regulates bone homeostasis in mice
Xiaoyu Li1, Lei Hu1, Yifan Xu1
1Salivary Gland Disease Center and Beijing Key Laboratory of Tooth Regeneration and Function Reconstruction, Beijing Laboratory of Oral Health and Beijing Stomatological Hospital, Capital Medical University, Beijing, China.
Bone Research
|February 9, 2026
Summary
Dietary nitrate and Sialin are crucial for mesenchymal stem cells (MSCs) function and bone health. Restoring Sialin with nitrate may prevent osteoporosis by improving mitochondrial energy in MSCs.
Area of Science:
- Cell Biology
- Biochemistry
- Physiology
Background:
- Mitochondrial regulation is key for mesenchymal stem cells (MSCs) in bone formation and skeletal homeostasis.
- Dietary nitrate and its transporter Sialin are known for systemic homeostasis but their role in MSCs is unclear.
Purpose of the Study:
- To investigate the role of Sialin in MSCs function and bone homeostasis.
- To elucidate the molecular mechanism by which Sialin influences osteogenic differentiation and mitochondrial bioenergetics.
Main Methods:
- Utilized gain- and loss-of-function studies to assess Sialin's impact on MSCs.
- Investigated Sialin's localization and its interaction with pSTAT3S727 in mitochondria.
- Examined the effect of dietary nitrate on Sialin expression and MSCs function in aged mice.
Main Results:
- Sialin deficiency impairs MSCs function and disrupts bone homeostasis.
- Sialin localizes to the mitochondrial membrane, promoting osteogenic differentiation by maintaining mitochondrial bioenergetic integrity.
- Sialin recruits pSTAT3S727 to mitochondria, forming a complex that enhances mitochondrial bioenergy and stabilizes bone remodeling.
- Dietary nitrate administration restored Sialin expression in aged mice, improving MSCs function and preventing osteoporosis.
Conclusions:
- Identified a novel nutrient-responsive signaling axis: nitrate-Sialin-pSTAT3S727.
- This axis promotes osteogenic differentiation through mitochondrial homeostasis.
- This pathway represents a potential therapeutic strategy for age-related osteoporosis.
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