中国神经再生研究(英文版) ›› 2026, Vol. 21 ›› Issue (4): 1396-1408.doi: 10.4103/NRR.NRR-D-24-01029

• 综述:脊髓损伤修复保护与再生 • 上一篇    下一篇

线粒体自噬:脊髓损伤病理生理和治疗的关键调节因子

  

  • 出版日期:2026-04-15 发布日期:2025-07-25

Mitophagy: A key regulator in the pathophysiology and treatment of spinal cord injury

Qiuyang Gu1, 2, #, Shengye Yuan1, 2, #, Yumei An2, #, Wenyue Sun2 , Mingyuan Xu2 , Mengchun Xue2 , Xianzhe Li2 , Chao Liu1 , Haiyan Shan3, *, Mingyang Zhang1, 2, *   

  1. 1 Department of Orthopedics, Suzhou BenQ Medical Center, Suzhou, Jiangsu Province, China;  2 Institute of Forensic Sciences, Suzhou Medical College, Suzhou, Jiangsu Province, China;  3 Department of Obstetrics and Gynecology, The Affiliated Suzhou Hospital of Nanjing Medical University, Suzhou, Jiangsu Province, China
  • Online:2026-04-15 Published:2025-07-25
  • Contact: Mingyang Zhang, MD, PhD, mingyangzhang@suda.edu.cn; Haiyan Shan MD, PhD, ghostqth@163.com.
  • Supported by:
    This work was supported by the National Natural Science Foundation of China, Nos. 82371389, 82071382 (to MZ); the Priority Academic Program Development of Jiangsu Higher Education Institutions, PAPD (to MZ); Jiangsu Maternal and Child Health Research Key Project, No. F202013 (to HS); Jiangsu 333 High Level Talent Training Project, 2022 (to HS); Gusu District Health Talent Training Project, No. 2024145 (to HS); Suzhou BenQ Medical Center Project, No. H220918 (to MZ); Undergraduate Training Program for Innovation and Entrepreneurship, Soochow University, No. 202410285091Z (to MZ).

摘要:

线粒体自噬与脊髓继发性损伤的发生密切相关。异常的线粒体自噬可能是继发性脊髓损伤的主要原因,可导致ATP生成障碍、离子失衡、活性氧过量产生、神经炎症和神经细胞死亡。因此,维持线粒体自噬的平衡可能对脊髓损伤的治疗至关重要。过度和不足的自噬都会阻碍损伤脊髓的恢复。此次综述总结了脊髓损伤的病理变化、线粒体自噬机制及线粒体自噬与脊髓损伤直接与间接的联系,然后介绍了靶向线粒体自噬治疗脊髓损伤的治疗方法,包括目前正在进行的的临床试验和其他新型疗法(干细胞、纳米新材料、小分子聚合物等新型药物),最后提出了目前在该领域遇到的问题并指明未来研究的可能方向。文章旨在为今后靶向调节线粒体自噬治疗脊髓损伤提供理论参考。

https://orcid.org/0000-0001-7084-6237 (Mingyang Zhang); https://orcid.org/0000-0002-6832-7363 (Haiyan Shan)

关键词: ATP生成障碍, 细胞死亡, 线粒体自噬, 神经炎症, 神经保护, 氧化应激, 继发性损伤, 脊髓损伤, 治疗

Abstract: Mitophagy is closely associated with the pathogenesis of secondary spinal cord injury. Abnormal mitophagy may contribute significantly to secondary spinal cord injury, leading to the impaired production of adenosine triphosphate, ion imbalance, the excessive production of reactive oxygen species, neuroinflammation, and neuronal cell death. Therefore, maintaining an appropriate balance of mitophagy is crucial when treating spinal cord injury, as both excessive and insufficient mitophagy can impede recovery. In this review, we summarize the pathological changes associated with spinal cord injury, the mechanisms of mitophagy, and the direct and indirect relationships between mitophagy and spinal cord injury. We also consider therapeutic approaches that target mitophagy for the treatment of spinal cord injury, including ongoing clinical trials and other innovative therapies, such as use of stem cells, nanomaterials, and small molecule polymers. Finally, we highlight the current challenges facing this field and suggest potential directions for future research. The aim of our review is to provide a theoretical reference for future studies targeting mitophagy in the treatment of spinal cord injury.

Key words: ATP production disorders, cell death, mitochondria, mitophagy, neuroinflammation, neuroprotection, oxidative stress, secondary injury, spinal cord injury, treatment