Tacrolimus may play a role in dermatitis and radiation-induced skin injury through cellular senescence  

作　　者：Jie Chen Ling Gao 

机构地区：[1]China CDC Key Laboratory of Radiological Protection and Nuclear Emergency,National Institute for Radiological Protection,Chinese Center for Disease Control and Prevention,Beijing 100088,China

出　　处：《Radiation Medicine and Protection》2024年第3期161-164,共4页放射医学与防护（英文）

基　　金：supported by the Beijing Municipal Natural Science Foundation(7202139 and 7162137),China.

摘　　要：Skin Exposure of skin to ionizing radiation can induce acute or chronic biological effects,resulting in radiation-induced skin injury(RSI).Premature cellular senescence,caused by oxidative stress and/or DNA damage from chemical or physical agents,leads to the decrease of cellular proliferation and physiological function.Persistent DNA damage and accumulation of senescent cells are associated with the progression of radiation-induced injury.Atopic dermatitis and RSI have similar inflammatory symptoms.The treatment of tacrolimus(TAC)in atopic dermatitis may be associated with premature cellular senescence.TAC can prevent the onset of cellular senes-cence by inactivating the p38 mitogen-activated protein kinase(p38 MAPK).The activation of p38 MAPK can induce the senescence-associated secretory phenotype(SASP)by enhancing the transcriptional activity of nuclear factor kappa-B(NF-κB),which ultimately leads to premature cellular senescence.FK506 binding protein 51(FKBP51)exhibits resistance to ionizing radiation,but the mechanism of TAC regulation of ionizing radiation-induced premature senescence still needs further study.This review discusses the mechanism of cellular senes-cence in RSI and the role of TAC in both dermatitis and RSI.

关 键 词：TACROLIMUS Premature cellular senescence Radiation-induced skin injury p38 MAPK NF-κB 

分 类 号：R339.38[医药卫生—人体生理学]