Yang Hailing, Ru Kang, Liu Shuai, Zhu Chunyu, Qian Airong, Chen Zhihao
Laboratory for Bone Metabolism, Xi'an Key Laboratory of Special Medicine and Health Engineering, Key Laboratory for Space Biosciences and Biotechnology, Research Center for Special Medicine and Health Systems Engineering, School of Life Sciences, Northwestern Polytechnical University, Xi'an 710129, China.
Department of Obstetrics and Gynecology, Xijing Hospital, The Fourth Military Medical University, Xi'an 710032, China.
Biology (Basel). 2025 Aug 15;14(8):1062. doi: 10.3390/biology14081062.
Ferroptosis, a distinct form of programmed cell death characterized by iron-dependent lipid peroxidation, has emerged as a critical factor in the pathogenesis of various diseases. Given the increasing prevalence of osteoporosis worldwide and the increasing incidence of osteoporosis, understanding the molecular mechanisms underlying bone loss is imperative for developing targeted therapies. Recent evidence suggests that ferroptosis plays a pivotal role in osteoporosis by influencing the balance between osteoblast and osteoclast activity. This review examines the mechanistic basis of ferroptosis and its pathological implications in osteoporosis. By delineating the interplay between ferroptosis and skeletal remodeling, we highlight potential therapeutic strategies aimed at modulating ferroptosis to mitigate osteoporosis progression.
铁死亡是一种独特的程序性细胞死亡形式,其特征是铁依赖性脂质过氧化,已成为各种疾病发病机制中的关键因素。鉴于全球骨质疏松症的患病率不断上升以及骨质疏松症的发病率不断增加,了解骨质流失的分子机制对于开发靶向治疗方法至关重要。最近的证据表明,铁死亡通过影响成骨细胞和破骨细胞活性之间的平衡在骨质疏松症中起关键作用。本综述探讨了铁死亡的机制基础及其在骨质疏松症中的病理意义。通过描述铁死亡与骨骼重塑之间的相互作用,我们强调了旨在调节铁死亡以减轻骨质疏松症进展的潜在治疗策略。