| 摘要: |
| ［摘要］ 骨质疏松症（OP）是一种全球流行的骨骼疾病，给社会带来沉重的健康与经济负担。同型半胱氨酸（Hcy）作为一种含硫氨基酸代谢中间产物，其血浆水平升高［即高同型半胱氨酸血症（HHcy）］已被确立为心脑血管疾病的独立危险因素。近年来，研究发现HHcy与骨密度降低、骨折风险增加及骨代谢紊乱密切相关，但其作用机制及临床意义仍存争议。该文系统阐述Hcy与OP关系的研究进展。首先，梳理流行病学证据，阐明Hcy水平与骨密度及骨折风险之间的复杂关系，并综述遗传多态性（如MTHFR基因）及B族维生素水平在此关联中的影响。其次，深入探讨其分子与细胞生物学机制，重点分析Hcy通过诱发氧化应激、炎症反应及干扰特定信号通路等途径破坏骨代谢平衡的核心作用。最后，该文评估了通过营养（补充叶酸、维生素B12等）及药物干预降低Hcy水平以防治OP的潜力与挑战。该文旨在为深入理解Hcy在OP发病中的作用提供全面视角，为研究OP新的防治策略提供理论依据。 |
| 关键词: 同型半胱氨酸 高同型半胱氨酸血症 骨质疏松症 骨代谢 骨密度 骨折风险 |
| DOI：10.3969/j.issn.1674-3806.2026.02.08 |
| 分类号:R 681 |
| 基金项目:国家自然科学基金项目（编号：82102608，82572729） |
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| Research progress in the relationships between homocysteine and osteoporosis |
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JIANG Shangkun1, YANG Lan2, LI Lijun3, LI Xinhua4
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1.School of Medicine, Tongji University, Shanghai 200092, China; 2.Department of General Practice, Shanghai General Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai 200080, China; 3.Department of Spinal Surgery, Shanghai East Hospital, Tongji University, Shanghai 200120, China; 4.Department of Orthopedics, Shanghai General Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai 200080, China
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| Abstract: |
| ［Abstract］ Osteoporosis(OP) is a globally prevalent skeletal disease that imposes a substantial health and economic burden on society.Homocysteine(Hcy), as a metabolic intermediate of sulfur-containing amino acids, has been confirmed as an independent risk factor for cardiovascular and cerebrovascular diseases when its plasma levels are elevated—a condition known as hyperhomocysteinemia(HHcy). In recent years, some researches have found that HHcy is closely associated with decreased bone mineral density, increased fracture risk and disordered bone metabolism. However, its mechanism of action and clinical significance remain controversial. This paper systematically reviews the research progress in the relationships between Hcy and OP. Firstly, it sorts out epidemiological evidence to clarify the complex relationships between Hcy levels and bone mineral density as well as fracture risk, and summarizes the effects of genetic polymorphisms(e.g., the MTHFR gene) and the levels of B vitamins on these relationships. Secondly, it deeply explores the molecular and cellular biological mechanisms, focusing on the core role of Hcy in disrupting bone metabolic balance via inducing oxidative stress and inflammatory responses, and interfering with specific signaling pathways. Finally, it evaluates the potential and challenges of reducing Hcy levels and preventing and treating OP through nutritional interventions(e.g., supplement with folic acid and vitamin B12) and pharmacological interventions. This review aims to provide a comprehensive perspective for a deeper understanding of the role of Hcy in the pathogenesis of OP and offers a theoretical basis for studying new prevention and treatment strategies for OP. |
| Key words: Homocysteine(Hcy) Hyperhomocysteinemia(HHcy) Osteoporosis(OP) Bone metabolism Bone mineral density Fracture risk |
