摘要
细胞早衰是指细胞在非端粒信号刺激下发生的增殖能力和生理功能下降,提前进入衰老状态。电离辐射可以引起细胞DNA损伤,随后经过细胞周期永久性停滞或启动SASP来诱导细胞早衰。其信号通路较为复杂,p53、p16、p38MAPK、p62等信号分子参与该过程。本文总结了辐射诱导p62介导的细胞早衰研究进展。
Premature cellular senescence refers to the decrease of proliferation and physiological function stimulated by non-telomere signals,promoting early aging.Ionizing radiation can cause DNA damage and induce premature cellular senescence by permanently halting the cell cycle or starting SASP signal factor.The signaling pathways of ionizing radiation-induced premature cellular senescence are complex and may include p53,p16,p38MAPK and p62.This review summarized the research progress of radiation-induced premature cellular senescence mediated by p62/SQSTM1.
作者
马丽萍
刘青杰
田梅
高玲
Ma Liping;Liu Qingjie;Tian Mei;Gao Ling(Key Laboratory of Radiological Protection and Nuclear Emergency,China CDC,National Institute for Radiological Protection,Chinese Center for Disease Control and Prevention,Beijing 100088,China)
出处
《中华放射医学与防护杂志》
CAS
CSCD
北大核心
2020年第12期968-972,共5页
Chinese Journal of Radiological Medicine and Protection
基金
国家自然科学基金(31570852,31570854)
北京市自然科学基金(7162137,7202139)。
