粒体自噬
脊髓
医学
脊髓损伤
缺血
神经科学
再灌注损伤
背景(考古学)
麻醉
自噬
心脏病学
生物
细胞凋亡
生物化学
精神科
古生物学
作者
Yanni Duan,Fengguang Yang,Yi-Bao Zhang,Mingtao Zhang,Yujun Shi,Yitian Lang,Hongli Sun,Xin Wang,Hongyun Jin,Xuewen Kang
标识
DOI:10.4103/nrr.nrr-d-24-00668
摘要
Spinal cord ischemia-reperfusion injury, a severe form of spinal cord damage, can lead to sensory and motor dysfunction. This injury often occurs after traumatic events, spinal cord surgeries, or thoracoabdominal aortic surgeries. The unpredictable nature of this condition, combined with limited treatment options, poses a significant burden on patients, their families, and society. Spinal cord ischemia-reperfusion injury leads to reduced neuronal regenerative capacity and complex pathological processes. In contrast, mitophagy is crucial for degrading damaged mitochondria, thereby supporting neuronal metabolism and energy supply. However, while moderate mitophagy can be beneficial in the context of spinal cord ischemia-reperfusion injury, excessive mitophagy may be detrimental. Therefore, this review aims to investigate the potential mechanisms and regulators of mitophagy involved in the pathological processes of spinal cord ischemia-reperfusion injury. The goal is to provide a comprehensive understanding of recent advancements in mitophagy related to spinal cord ischemia-reperfusion injury and clarify its potential clinical applications.
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