Research progress of ferroptosis in the mechanism and treatment of osteoporosis

doi:10.3877/cma.j.issn.2096-0263.2026.03.008

Abstract

Abstract:

Osteoporosis (OP) is a common disease in the elderly, which is characterized by decreased bone strength, decreased bone mineral density and increased risk of fracture. It is mainly caused by the imbalance of bone remodeling, that is, bone resorption caused by osteoclasts exceeds bone synthesis. Ferroptosis is an iron-dependent regulatory cell death mode caused by lipid peroxidation. Intracellular divalent iron ions (Fe²⁺) produce a large number of iron-dependent reactive oxygen species through REDOX reactions, which promote lipid peroxidation and lead to cell death. At present, the role and detailed mechanism of ferroptosis in the development of OP have not been fully elucidated. Ferroptosis may be mediated by glutathione peroxidase 4(GPX4), iron overload and lipid peroxidation affect osteoblasts and osteoclasts to accelerate the progression of OP. Based on the theory of ferroptosis, this review further discusses the role of ferroptosis in the development of OP and potential therapeutic targets, in order to provide new strategies and directions for the diagnosis and treatment of OP and drug research and development.

Key words: Ferroptosis, Osteoporosis, Osteoblasts, Osteoclasts

Wenbin Bao, Chenlu An, Qing Chang, Qiang Li, Jianmin Zhao. Research progress of ferroptosis in the mechanism and treatment of osteoporosis[J]. Chinese Journal of Geriatric Orthopaedics and Rehabilitation(Electronic Edition), 2026, 12(03): 180-187.

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References 68

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骨质疏松类型	核心病理机制与铁死亡的关系	关键分子/信号通路	干预策略与潜在药物
绝经后骨质疏松症	雌激素缺乏+铁过载→氧化应激→成骨细胞铁死亡。铁死亡通过激活破骨细胞加剧骨流失。	核心轴：GPX4（关键酶，受雌激素调节）、SLC7A11/GSH 调控通路：KEAP1/NRF2/HMOX1、PI3K/Akt（circRNA/miR轴）	纳米材料：包被DFO/咖啡酸的纳米球天然化合物：女贞子（Nrf2/HO-1）、知母-黄柏靶向基因：PTEN，SIRT1等
糖皮质激素诱导的骨质疏松症	GC长期使用→直接/间接诱导成骨细胞铁死亡。铁死亡是其骨质流失的关键驱动因素。	保护性通路：Nrf2/GPX4、PI3K/AKT/mTOR 细胞通讯：外泌体介导的保护作用	天然产物：秦皮素（Fraxin，激活Nrf2/GPX4）内源性激素：褪黑素（MT，激活PI3K/AKT/mTOR），即使启动后仍有效外泌体疗法：血管内皮/内皮祖细胞来源的外泌体（抑制铁自噬）
糖尿病性骨质疏松症	高糖环境→多条信号通路紊乱→诱导成骨细胞铁死亡。	诱导通路：HIF1α、METTL3/ASK1-p38 保护通路：Nrf2/GPX4、AMPK/SIRT1、HO-1、PCBP1（促进铁蛋白表达）	维生素D：Eldecalcitol（ED- 71，激活HIF1α）天然产物：地黄苷（Pol）、灰毡毛忍冬皂苷（AVI）、姜黄素纳米递送：四面体框架核酸（tFNA）递送姜黄素
其他类型骨质疏松症	吸烟（SROP）：烟草毒素积累→诱导BMSC铁死亡和铁自噬。年龄相关性：衰老相关应激→成骨细胞铁死亡。	SROP关键因子：铁自噬、ROS相关通路年龄相关关键因子：ATF3（骨细胞铁死亡驱动因子）	SROP：骨靶向工程外泌体递送姜黄素年龄相关：维生素D受体激活（Nrf2/GPX4）、抑制ATF3

骨质疏松类型	核心病理机制与铁死亡的关系	关键分子/信号通路	干预策略与潜在药物
绝经后骨质疏松症	雌激素缺乏+铁过载→氧化应激→成骨细胞铁死亡。铁死亡通过激活破骨细胞加剧骨流失。	核心轴：GPX4（关键酶，受雌激素调节）、SLC7A11/GSH 调控通路：KEAP1/NRF2/HMOX1、PI3K/Akt（circRNA/miR轴）	纳米材料：包被DFO/咖啡酸的纳米球天然化合物：女贞子（Nrf2/HO-1）、知母-黄柏靶向基因：PTEN，SIRT1等
糖皮质激素诱导的骨质疏松症	GC长期使用→直接/间接诱导成骨细胞铁死亡。铁死亡是其骨质流失的关键驱动因素。	保护性通路：Nrf2/GPX4、PI3K/AKT/mTOR 细胞通讯：外泌体介导的保护作用	天然产物：秦皮素（Fraxin，激活Nrf2/GPX4）内源性激素：褪黑素（MT，激活PI3K/AKT/mTOR），即使启动后仍有效外泌体疗法：血管内皮/内皮祖细胞来源的外泌体（抑制铁自噬）
糖尿病性骨质疏松症	高糖环境→多条信号通路紊乱→诱导成骨细胞铁死亡。	诱导通路：HIF1α、METTL3/ASK1-p38 保护通路：Nrf2/GPX4、AMPK/SIRT1、HO-1、PCBP1（促进铁蛋白表达）	维生素D：Eldecalcitol（ED- 71，激活HIF1α）天然产物：地黄苷（Pol）、灰毡毛忍冬皂苷（AVI）、姜黄素纳米递送：四面体框架核酸（tFNA）递送姜黄素
其他类型骨质疏松症	吸烟（SROP）：烟草毒素积累→诱导BMSC铁死亡和铁自噬。年龄相关性：衰老相关应激→成骨细胞铁死亡。	SROP关键因子：铁自噬、ROS相关通路年龄相关关键因子：ATF3（骨细胞铁死亡驱动因子）	SROP：骨靶向工程外泌体递送姜黄素年龄相关：维生素D受体激活（Nrf2/GPX4）、抑制ATF3

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