郭肖可,汪晓妹

近年来，2型糖尿病（T2DM）与骨质疏松（OP）的交互作用研究聚焦于血红蛋白（Hb）的动态变化及其在骨代谢中的双重角色。分子机制揭示，慢性高血糖通过晚期糖基化终末产物（AGEs）沉积、铁死亡及氧化应激轴，导致Hb年均下降1.2 g/L，而Hb降低通过骨髓缺氧-HIF-1α通路激活破骨分化，形成“血糖-Hb-骨质量”恶性循环。临床研究显示，中国T2DM患者Hb与骨密度（BMD）的关联强度显著高于欧美人群，且Hb波动较静态低Hb值更敏感预测BMD丢失。治疗策略中，基于Hb的分层干预显示：HbA1c>9%且Hb<120 g/L时，促红细胞生成素（EPO）联合双膦酸盐治疗使腰椎BMD提升41%；二甲双胍需动态监测Hb水平。创新技术如AI多模态预测模型（骨折风险预测准确率89.3%）及CRISPR-dCas9靶向调控SOD2抗氧化通路为精准干预提供新工具。未来需深入探索Hb时空波动阈值、性别特异性铁代谢调控（如XIST lncRNA-m6A修饰）及多组学整合策略，以破解T2DM-OP共病的分子网络，推动个体化诊疗体系发展。

2型糖尿病；血红蛋白；骨质疏松；铁死亡；精准医疗

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