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由HDAC3异常引起的GPX4抑制驱动脏铁亡和AKI-CKD进展

Lijun Zhang1, Fang Chen2, Jian Dong3

  • 1Yancheng Medical Research Center of Nanjing University Medical School, Department of Central Laboratory, Yancheng First Hospital, Affiliated Hospital of Nanjing University Medical School, The First People's Hospital of Yancheng, Yancheng, China; Nanjing University Medical School, Jiangsu Key Lab of Molecular Medicine, Nanjing, China.

Redox biology
|October 27, 2023
PubMed
概括

基因素脱乙酶3 (HDAC3) 异常驱动铁和病的进展,通过抑制GPX4. 抑制HDAC3可以保护GPX4,减少铁亡并减缓急性病转变为慢性病.

关键词:
AKI-CKD的进展情况.铁性化 (ferroptosis) 是一种在GPX4中使用GPX4.在 HDAC3 中,HDAC3 是在KLF5KLF5KLF5KLF5

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