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| 骨骼肌线粒体DNA释放介导的cGAS-STING通路在肌少-骨质疏松症中的研究进展 |
| Mitochondrial DNA release-mediated cGAS-STING pathway in skeletal muscle advances in sarcopen-osteoporosis research |
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| DOI：10.3969/j.issn.1006-7108.2026.06.022 |
| 中文关键词: cGAS-STING通路 线粒体mtDNA 肌少-骨质疏松症 |
| 英文关键词:cGAS-STING pathway mtDNA sarcopen-osteoporosis |
| 基金项目:甘肃省卫生健康行业科研计划项目（GSWSKY2021-035） |
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| 中文摘要: |
| 肌少-骨质疏松症是以骨骼肌质量/功能减退与骨量丢失协同恶化为特征的代谢性疾病，其病理机制涉及线粒体稳态失衡、表观遗传调控异常及炎症微环境重塑等多维度调控网络。因氧化应激、自噬及机械损伤等导致骨骼肌线粒体损伤引发的线粒体DNA（mtDNA）异常释放及其介导的cGAS-STING通路的激活，通过调控成肌分化抑制因子（如STAT1/IRF2）和成骨细胞分化关键信号（如Wnt/β-catenin），同时激活破骨细胞分化通路（如 RANKL/NF-KB），形成“炎症-线粒体损伤-肌骨共病”恶性循环。靶向 mtDNA释放或cGAS-STING信号轴有望成为改善肌少症-骨质疏松症的新兴靶点。 |
| 英文摘要: |
| Sarcopenia-osteoporosis is a metabolic disease characterized by the synergistic deterioration of skeletal muscle mass/function loss and bone loss, and its pathological mechanism involves multi-dimensional regulatory networks such as mitochondrial homeostasis imbalance, abnormal epigenetic regulation, and inflammatory microenvironment remodeling. The abnormal release of mitochondrial DNA (mtDNA) caused by mitochondrial damage in skeletal muscle caused by oxidative stress, autophagy, and mechanical damage and the activation of the cGAS-STING pathway mediated by regulating myogenic differentiation inhibitors (e.g., STAT1/IRF2) and key signals of osteoblast differentiation (e.g., Wnt/B-catenin), and activate osteoclast differentiation pathways (e.g., RANKL/NF-KB), forming a vicious cycle of "inflammation-mitochondrial damage-musculoskeletal comorbidity". Targeting mtDNA release or cGAS-STING signaling axis is expected to be an emerging target for the improvement of sarcopenia-osteoporosis. |
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