SIRT3
粒体自噬
氧化应激
脊髓损伤
生物
线粒体
细胞生物学
SOD2
神经科学
脊髓
自噬
锡尔图因
内分泌学
生物化学
细胞凋亡
乙酰化
超氧化物歧化酶
基因
作者
Dechun Jiang,Xu Yang,Minghao Ge,Hengshuo Hu,Chang Xu,Shan Wen,Hao Deng,Xifan Mei
摘要
Spinal cord injury (SCI) is a central nervous system injury that is primarily traumatic and manifests as motor, sensory, and autonomic dysfunction below the level of damage. Our previous studies confirmed the ability of zinc to protect mitochondria, protect neurons and promote spinal cord recovery. However, the role of zinc in Parthanatos is unknown.We investigated the effects of zinc in Parthanatos from oxidative stress and mitophagy. We elucidated the role of SIRT3 in providing new ideas for treating spinal cord injury.Zinc protected SCI mice by regulating Parthanatos. On the one hand, zinc eliminated ROS directly through SIRT3 deacetylation targeting SOD2 to alleviate Parthanatos. On the other hand, zinc eliminated ROS indirectly through SIRT3-mediated promotion of mitophagy to alleviate Parthanatos.Zinc defends against Parthanatos and promotes functional recovery after spinal cord injury through SIRT3-mediated anti-oxidative stress and mitophagy.
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