Journal
BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS
Volume 519, Issue 2, Pages 240-245Publisher
ACADEMIC PRESS INC ELSEVIER SCIENCE
DOI: 10.1016/j.bbrc.2019.08.165
Keywords
Acute radiation-induced lung injury; Glutathione peroxidase 4; Ferroptosis; Reactive oxygen species
Categories
Funding
- National Natural Science Foundation of China of China [81800079]
- Jinshan Health Planning Committee Fund [JSKJ-KTQN-2017-01]
Ask authors/readers for more resources
Radiation-induced lung injury (RILI) is one of the most common and fatal complications of thoracic radiotherapy. Cell death is the critical point in RILI. Ferroptosis is discovered recently as a new type of cell death which is different from other forms. Our research investigated the role of ferroptosis in the process of acute RILI in mice. The levels of ROS in lungs and the inflammatory cytokine levels (TNF-alpha, IL-6, IL-10, and TGF-beta 1) in serum decreased significantly post ferroptosis inhibitor treatment in acute RILI. Ferroptotic characteristic changes of mitochondria in acute RILI was observed by transmission electron microscopy (TEM). Treatment with ferroptosis inhibitor significantly alleviated radiation-induced histopathological changes in mice lungs. Glutathione peroxidase 4 (GPX4), the key maker of the ferroptosis, was down-regulated in RILI. In summary, we observed that ferroptosis played a crucial role in acute RILI, and the ROS induced by irradaition might be the original trigger of ferroptosis in acute RILI. At the same time, ferroptosis may also affect the levels of inflammatory cytokines in acute RILI. (C) 2019 The Authors. Published by Elsevier Inc.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available