Correction: Drp1 regulates mitochondrial dysfunction and dysregulated metabolism in ischemic injury via Clec16a-, BAX-, and GSH- pathways.
作者信息
Duan Chenyang, Kuang Lei, Xiang Xinming, Zhang Jie, Zhu Yu, Wu Yue, Yan Qingguang, Liu Liangming, Li Tao
机构信息
State Key Laboratory of Trauma, Burns and Combined Injury, Second Department of Research Institute of Surgery, Daping Hospital, Army Medical University, 400042, Chongqing, PR China.
出版信息
Cell Death Dis. 2025 Jan 13;16(1):11. doi: 10.1038/s41419-024-07314-0.
Abstract
摘要
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Correction: Drp1 regulates mitochondrial dysfunction and dysregulated metabolism in ischemic injury via Clec16a-, BAX-, and GSH- pathways.更正：动力相关蛋白1（Drp1）通过Clec16a、BAX和谷胱甘肽（GSH）途径调节缺血性损伤中的线粒体功能障碍和代谢失调。
Cell Death Dis. 2025 Jan 13;16(1):11. doi: 10.1038/s41419-024-07314-0.
2
Correction: Drp1 regulates mitochondrial dysfunction and dysregulated metabolism in ischemic injury via Clec16a-, BAX-, and GSH- pathways.更正：动力相关蛋白1（Drp1）通过Clec16a、BAX和谷胱甘肽（GSH）途径调节缺血性损伤中的线粒体功能障碍和代谢失调。
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Drp1 regulates mitochondrial dysfunction and dysregulated metabolism in ischemic injury via Clec16a-, BAX-, and GSH- pathways.Drp1 通过 Clec16a、BAX 和 GSH 途径调节缺血性损伤中的线粒体功能障碍和代谢失调。
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Bax/Bak promote sumoylation of DRP1 and its stable association with mitochondria during apoptotic cell death.在凋亡性细胞死亡过程中，Bax/Bak促进动力相关蛋白1（DRP1）的SUMO化修饰及其与线粒体的稳定结合。
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Drp1 acetylation mediated by CDK5-AMPK-GCN5L1 axis promotes cerebral ischemic injury via facilitating mitochondrial fission.DRP1 乙酰化通过 CDK5-AMPK-GCN5L1 轴促进脑缺血损伤，通过促进线粒体分裂。
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