Sialin-STAT3軸はマウスの骨恒常性を調節する

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Updated: Feb 11, 2026

Author Spotlight: Comparing Alveolar and Long Bone Remodeling to Explore OTM Model Potential

Author Spotlight: Comparing Alveolar and Long Bone Remodeling to Explore OTM Model Potential

Published on: July 21, 2023

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.

|February 9, 2026

Abstract:

Mitochondrial regulation in mesenchymal stem cells (MSCs) serves as a critical determinant of bone formation and skeletal homeostasis. While dietary nitrate and its transporter Sialin are implicated in systemic homeostasis, their specific roles in MSCs' function remain unclear. Here, we demonstrate that Sialin deficiency impairs MSCs' function and disrupts bone homeostasis. Gain- and loss-of-function studies reveal that Sialin localizes to the mitochondrial membrane and promotes osteogenic differentiation by maintaining mitochondrial bioenergetic integrity. Mechanistically, Sialin recruits pSTAT3^S727 to mitochondria, forming a functional complex that activates mitochondrial bioenergy and stabilizes bone remodeling. Notably, dietary nitrate restores Sialin expression in aged mice, thereby enhancing MSCs' function and preventing osteoporosis. Our findings identify a nutrient-responsive signaling axis-nitrate-Sialin-pSTAT3^S727-that promotes osteogenic differentiation via mitochondrial homeostasis, offering a potential therapeutic strategy for age-related osteoporosis.

キーワード:

間葉系幹細胞骨粗鬆症ミトコンドリア硝酸塩 Sialin STAT3 骨恒常性骨形成シグナル伝達老化

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Skeletal Phenotype Analysis of a Conditional Stat3 Deletion Mouse Model

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Mechanism of Regulation of Adipocyte Numbers in Adult Organisms Through Differentiation and Apoptosis Homeostasis

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