Nrf-2 as a novel target in radiation induced lung injury

被引:5
作者
Chen, Yuan-Yuan [1 ]
Wang, Meng [1 ]
Zuo, Chen-Yang [1 ]
Mao, Meng-Xia [1 ]
Peng, Xiao-Chun [2 ,3 ]
Cai, Jun [1 ]
机构
[1] Yangtze Univ, Affiliated Hosp 1, Dept Oncol, Nanhuan Rd, Jingzhou 434023, Hubei, Peoples R China
[2] Yangtze Univ, Sch Basic Med, Ctr Mol Med, Lab Oncol,Hlth Sci Ctr, Jingzhou 434023, Hubei, Peoples R China
[3] Yangtze Univ, Hlth Sci Ctr, Sch Basic Med, Dept Pathophysiol, Nanhuan Rd, Jingzhou 434023, Hubei, Peoples R China
关键词
RILI; Nrf-2; Inflammatory response; Fibrosis; Ferroptosis; EPITHELIAL-MESENCHYMAL TRANSITION; ERYTHROID 2-RELATED FACTOR-2; TRANSCRIPTION FACTOR NRF2; OXIDATIVE STRESS; SIGNALING PATHWAY; DNA-DAMAGE; NRF2-MEDIATED ANTIOXIDANT; ENHANCES SUSCEPTIBILITY; NF-E2-RELATED FACTOR-2; CDDO-IMIDAZOLIDE;
D O I
10.1016/j.heliyon.2024.e29492
中图分类号
O [数理科学和化学]; P [天文学、地球科学]; Q [生物科学]; N [自然科学总论];
学科分类号
07 ; 0710 ; 09 ;
摘要
Radiation-induced lung injury (RILI) is a common and fatal complication of chest radiotherapy. The underlying mechanisms include radiation-induced oxidative stress caused by damage to the deoxyribonucleic acid (DNA) and production of reactive oxygen species (ROS), resulting in apoptosis of lung and endothelial cells and recruitment of inflammatory cells and myofibroblasts expressing NADPH oxidase to the site of injury, which in turn contribute to oxidative stress and cytokine production. Nuclear factor erythroid 2-related factor 2 (Nrf-2) is a vital transcription factor that regulates oxidative stress and inhibits inflammation. Studies have shown that Nrf-2 protects against radiation-induced lung inflammation and fibrosis. This review discusses the protective role of Nrf-2 in RILI and its possible mechanisms.
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页数:12
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