转录因子ATF3调解SOCS3表达通过激活线粒细胞衰变会加剧脏缺血-再输液损伤
Yu Luo1,2, Zhitao Cai2, Xiongfei Wu2
1Department of Urology, Wuhan Sixth Hospital Affiliated Hospital of Jianghan University, Wuhan, China.
Nephron
|November 13, 2023
概括
细胞因子信号传递3 (SOCS3) 抑制剂通过促进线粒细胞衰变而加剧损伤. 激活转录因子3 (ATF3) 驱动SOCS3的表达,恶化脏缺血症/再输液损伤.
科学领域:
- 腎臟病學 (nephrology) 是一種醫學專業.
- 分子生物学分子生物学
- 细胞生物学 细胞生物学
背景情况:
- 缺血/再输液 (RI/R) 损伤是一个重大的临床挑战.
- 细胞因子信号传递3抑制剂 (SOCS3) 与RI/R损伤和线粒细胞衰变调节有关.
研究的目的:
- 研究SOCS3通过线粒调节影响RI/R损伤的机制.
- 在RI/R损害的背景下,确定SOCS3的上游调节者.
主要方法:
- 已建立的RI/R小鼠和低氧/低氧化 (H/R) 细胞模型.
- 通过生物化学测定,分子生物学技术和组织学分析评估损伤和线粒.
- 通过数据库分析和各种绑定测试,确定并验证了ATF3,SOCS3和IGF1R之间的相互作用.
主要成果:
- RI/R损伤模型显示BUN和肌素水平升高,证实成功诱导.
- 在RI/R小鼠中,SOCS3的表达被上调;沉默SOCS3减轻了损伤和抑制了线粒.
- 激活转录因子3 (ATF3) 被确定为直接结合SOCS3促进体,影响其表达.
结论:
- ATF3调解SOCS3的表达,促进线粒并加剧RI/R损伤.
- 针对ATF3-SOCS3通路可能为RI/R损伤提供治疗策略.
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