在脊髓伤后的微质中,ACOD1,而不是伊塔科纳酸,促进了p62介导的Nrf2的激活

Zhanyang Qian1, Mingjie Xia2, Tianyu Zhao1,3

  • 1Department of Orthopedics, Taizhou School of Clinical Medicine, Taizhou People's Hospital of Nanjing Medical University, Nanjing Medical University, Taizhou, China.

概括

甲酸脱碳酶1 (ACOD1) 通过减少神经炎症和氧化应激来保护脊髓损伤 (SCI). 一个新的ACOD1-p62-Nrf2反循环增强神经保护,与伊塔科纳特不同.