Department of Orthopedics, the Affiliated Lianyungang Hospital of Xuzhou Medical University (The First People's Hospital of Lianyungang), Lianyungang, China.
Department of Orthopedics, Northern Jiangsu People's Hospital Affiliated to Yangzhou University/Clinical Medical College, Yangzhou University, Yangzhou, China.
Front Immunol. 2024 Jan 23;15:1330678. doi: 10.3389/fimmu.2024.1330678. eCollection 2024.
The damage to the central nervous system and dysfunction of the body caused by spinal cord injury (SCI) are extremely severe. The pathological process of SCI is accompanied by inflammation and injury to nerve cells. Current evidence suggests that oxidative stress, resulting from an increase in the production of reactive oxygen species (ROS) and an imbalance in its clearance, plays a significant role in the secondary damage during SCI. The transcription factor nuclear factor erythroid 2-related factor 2 (Nrf2) is a crucial regulatory molecule for cellular redox. This review summarizes recent advancements in the regulation of ROS-Nrf2 signaling and focuses on the interaction between ROS and the regulation of different modes of neuronal cell death after SCI, such as apoptosis, autophagy, pyroptosis, and ferroptosis. Furthermore, we highlight the pathways through which materials science, including exosomes, hydrogels, and nanomaterials, can alleviate SCI by modulating ROS production and clearance. This review provides valuable insights and directions for reducing neuronal cell death and alleviating SCI through the regulation of ROS and oxidative stress.
脊髓损伤（SCI）会对中枢神经系统造成严重损害，并导致身体机能障碍。SCI 的病理过程伴随着神经细胞的炎症和损伤。目前的证据表明，氧化应激在 SCI 的继发性损伤中起重要作用，其产生是由于活性氧（ROS）的产生增加和清除失衡所致。转录因子红细胞生成 2 相关因子 2（Nrf2）是细胞内氧化还原的关键调节分子。本综述总结了 ROS-Nrf2 信号转导的最新研究进展，并重点关注了 ROS 与 SCI 后不同神经元细胞死亡方式（凋亡、自噬、细胞焦亡和铁死亡）的调节之间的相互作用。此外，我们还强调了材料科学（包括外泌体、水凝胶和纳米材料）通过调节 ROS 的产生和清除来缓解 SCI 的途径。本综述为通过调节 ROS 和氧化应激来减少神经元细胞死亡和缓解 SCI 提供了有价值的见解和方向。
