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| TLR4介导信号网络调控骨质疏松症研究进展 |
| New progress in the study of TLR4 mediated signaling network regulation of osteoporosis |
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| DOI:10.3969/j.issn.1006-7108.2026.08.023 |
| 中文关键词: 骨质疏松症 骨代谢 Toll样受体4 信号网络 |
| 英文关键词:osteoporosis bone metabolism toll-like receptor 4 signaling network |
| 基金项目:国家自然科学基金项目(81660762);贵州省中医药管理局科技项目(QZYY-2021-022) |
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| 中文摘要: |
| 骨质疏松是一种代谢性骨骼退行性疾病,慢性炎症引起的骨代谢失衡使骨组织微结构损坏,而这种病理性骨损伤是骨质疏松患者骨质流失不可逆性增加的直接原因。Toll样受体4(TLR4)在破骨细胞增殖与骨量减少、成骨细胞与骨细胞凋亡以及骨形成与骨吸收比值失衡等骨质疏松病理过程中发挥关键的调控作用,故TLR4及其介导的信号网络调控骨质疏松已成为近年来研究的热点。本文从NF-κB、Wnt、RANKL、TRAF6以及TNF-α等信号靶点的角度综述TLR4调控骨质疏松的分子机制,为骨质疏松机制研究与新药研发提供理论依据。 |
| 英文摘要: |
| Osteoporosis, a systemic metabolic bone disease characterized by compromised bone strength, arises from an imbalance in bone metabolism often triggered by chronic inflammation, leading to microstructural deterioration of the bone tissue. This pathological bone damage is a primary cause of the irreversible increase in bone loss observed in osteoporosis patients. Toll-like receptor 4 (TLR4), a key component of the innate immune system, plays a critical regulatory role in the pathogenesis of osteoporosis, influencing osteoclast proliferation and consequent bone loss, osteoblast and osteocyte apoptosis, and the imbalance between bone formation and resorption. Consequently, the regulatory role of TLR4 and its downstream signaling networks in osteoporosis has become a prominent research focus in recent years. This review comprehensively summarizes the molecular mechanisms through which TLR4 regulates osteoporosis, focusing on key signaling targets such as NF-κB, Wnt/β-catenin, RANKL, TRAF6, and TNF-α. The insights presented herein provide a theoretical framework for advancing our understanding of osteoporosis pathogenesis and for the development of novel therapeutic interventions. |
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