Guo Yue, Zhang Jing, Gong Luyu, Liu Na, Liu Qiaoqiao, Liu Zhaojun, Guo Baosheng, Yang Jingping
Jiangsu Key Laboratory of Molecular Medicine, Medical School, Nanjing University, Nanjing 210093, China.
Antioxidants (Basel). 2025 Mar 15;14(3):346. doi: 10.3390/antiox14030346.
The mechano-responsiveness of osteocytes is critical for maintaining bone health and associated with a reduced oxidative stress defense, yet the precise molecular mechanisms remain incompletely understood. Here, we address the gap by investigating the epigenetic reprogramming that drives osteocyte responses to mechanical loading. We found overall remodeling of antioxidant response under mechanical loading and identified NRF2, a key transcription factor in oxidative stress response, which plays a vital role in the epigenetic remodeling of osteocytes. The results showed that mechanical loading enhanced NRF2 protein stability, promoted its nuclear translocation, and activated osteocyte-specific transcriptional programs. In contrast, pharmacological stabilization of NRF2 failed to fully replicate these effects, underscoring the unique role of mechanical stimuli in modulating NRF2 activity and antioxidant function. Our findings highlight the potential therapeutic limitations of NRF2-stabilizing drugs and suggest that combining pharmacological approaches with mechanical interventions could offer more effective treatments to maintain oxidative homeostasis.
骨细胞的机械反应性对于维持骨骼健康至关重要,且与氧化应激防御能力降低有关,但其确切的分子机制仍未完全明确。在此,我们通过研究驱动骨细胞对机械负荷作出反应的表观遗传重编程来填补这一空白。我们发现机械负荷下抗氧化反应发生了整体重塑,并鉴定出氧化应激反应中的关键转录因子NRF2,其在骨细胞的表观遗传重塑中起着至关重要的作用。结果表明,机械负荷增强了NRF2蛋白的稳定性,促进其核转位,并激活了骨细胞特异性转录程序。相比之下,NRF2的药理学稳定作用未能完全复制这些效应,这突出了机械刺激在调节NRF2活性和抗氧化功能方面的独特作用。我们的研究结果凸显了NRF2稳定药物潜在的治疗局限性,并表明将药理学方法与机械干预相结合可能会提供更有效的治疗方法来维持氧化稳态。