Li Pan, Xu Tian-Yang, Yu Ao-Xue, Liang Jing-Ling, Zhou Ya-Shuang, Sun Huai-Zhu, Dai Yu-Lin, Liu Jia, Yu Peng
College of Pharmacy, Changchun University of Chinese Medicine, Jilin 130117, China.
Innovation Practice Center, Changchun University of Chinese Medicine, Jilin 130117, China.
Biology (Basel). 2025 Apr 2;14(4):367. doi: 10.3390/biology14040367.
OP, a systemic bone disorder marked by reduced bone mass and heightened fracture risk, poses a significant global health burden, particularly among aging populations. Current treatments, including bisphosphonates and calcium supplementation, are limited by adverse effects and incomplete efficacy. Emerging research highlights ferroptosis-an iron-dependent cell death driven by lipid peroxidation-as a critical contributor to OP pathogenesis, characterized by dysregulated iron metabolism, oxidative stress, and lipid peroxide accumulation, which disrupt bone remodeling by impairing osteoblast function and enhancing osteoclast activity. This review elucidates the mechanistic interplay between ferroptosis and OP subtypes (diabetic osteoporosis (DOP), glucocorticoid-induced (GIOP), and postmenopausal osteoporosis (PMOP)) and evaluates the efficacy of Chinese herbal interventions in mitigating ferroptosis-driven bone loss. Key findings reveal that excess iron exacerbates lipid peroxidation via the Fenton reaction, while glutathione peroxidase 4 (GPX4) inactivation and system Xc- inhibition amplify oxidative damage. In DIOP, hyperglycemia-induced ROS and advanced glycation end products suppress osteogenesis, countered by melatonin and naringenin via nuclear factor -related factor 2 (Nrf2)/GPX4 activation. GIOP involves dexamethasone-mediated GPX4 downregulation, mitigated by exosomes and melatonin through phosphatidylinositol 3-kinase (PI3K)/protein kinase B (AKT)/mammalian target of rapamycin (mTOR) signaling. PMOP driven by estrogen deficiency-induced iron overload is alleviated by aconitine and icariin (ICA) via nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) and signal transducer and activator of transcription 3 (STAT3) pathways. Chinese herbs, including active compounds (quercetin, gastrodin, ICA, etc.) and formulations (Bugu Shengsui Capsule, Erxian Decoction (EXD), etc.), regulate iron metabolism, enhance antioxidant defenses (Nrf2/heme oxygenase 1(HO-1)), and inhibit lipid peroxidation, effectively restoring bone homeostasis. These findings underscore ferroptosis as a pivotal mechanism in OP progression and highlight the therapeutic promise of Chinese herbs in bridging traditional medicine with modern mechanistic insights. Future research should prioritize elucidating precise molecular targets, optimizing formulations, and validating clinical efficacy to address current therapeutic gaps.
骨质疏松症(OP)是一种全身性骨骼疾病,其特征为骨量减少和骨折风险增加,给全球健康带来了重大负担,在老年人群体中尤为突出。目前的治疗方法,包括双膦酸盐和补充钙,受到副作用和疗效不完全的限制。新兴研究强调铁死亡——一种由脂质过氧化驱动的铁依赖性细胞死亡——是OP发病机制的关键因素,其特征是铁代谢失调、氧化应激和脂质过氧化物积累,通过损害成骨细胞功能和增强破骨细胞活性来破坏骨重塑。这篇综述阐明了铁死亡与OP亚型(糖尿病性骨质疏松症(DOP)、糖皮质激素诱导的骨质疏松症(GIOP)和绝经后骨质疏松症(PMOP))之间的机制相互作用,并评估了中药干预减轻铁死亡驱动的骨质流失的疗效。主要研究结果表明,过量的铁通过芬顿反应加剧脂质过氧化,而谷胱甘肽过氧化物酶4(GPX4)失活和系统Xc-抑制会放大氧化损伤。在DOP中,高血糖诱导的活性氧(ROS)和晚期糖基化终产物抑制成骨作用,褪黑素和柚皮苷通过核因子相关因子2(Nrf2)/GPX4激活来对抗这种作用。GIOP涉及地塞米松介导的GPX4下调,外泌体和褪黑素通过磷脂酰肌醇3激酶(PI3K)/蛋白激酶B(AKT)/雷帕霉素哺乳动物靶蛋白(mTOR)信号通路来减轻这种下调。由雌激素缺乏诱导的铁过载驱动的PMOP可通过乌头碱和淫羊藿苷(ICA)通过活化B细胞的核因子κ轻链增强子(NF-κB)和信号转导及转录激活因子3(STAT3)途径得到缓解。中药,包括活性成分(槲皮素、天麻素、ICA等)和方剂(补骨生髓胶囊、二仙汤(EXD)等),调节铁代谢,增强抗氧化防御(Nrf2/血红素加氧酶1(HO-1)),并抑制脂质过氧化,有效恢复骨稳态。这些发现强调铁死亡是OP进展中的关键机制,并突出了中药在将传统医学与现代机制见解相结合方面的治疗前景。未来的研究应优先阐明精确的分子靶点、优化方剂并验证临床疗效,以填补当前的治疗空白。