The role of NLRP3 inflammasome activation in radiation damage

Abstract

Radiotherapy (RT) is currently one of the leading treatment for various cancers and it may cause injury to healthy tissue, with both short-term and long-term side effects. Inflammatory responses play an important role in the adverse reactions of early and late ionizing radiation. Nucleotide-binding domain and leucine-rich-repeat-containing family pyrin 3 (NLRP3) inflammasome as a multi-protein complex that activates caspase-1 can give rise to the proinflammatory cytokines such as interleukin-18 (IL-18) and interleukin-1 beta (IL-1β) maturation. Recent experiments and studies have shown that up-regulation of NLRP3 inflammasome have a big impact on radiation damage, which include radiation-induced oral mucositis, radiation-induced skin reactions, radiation-induced lung damage, radiation-induced intestinal injury and radiation-induced changes in other systems. In this paper, we will review the role of NLRP3 inflammasome in radiation damage, to explore possible therapeutic strategies for radiation damage.

Keywords

• NLRP3 inflammasome
• Radiotherapy
• Radiation damage
• Inflammatory signaling pathway
• IL-1β
• ROS