Ferroptosis, autophagy, pyroptosis, and necroptosis in the occurrence and development of radiation-induced lung injury

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Abstract

Radiation-induced lung injury (RILI) is one of the side effects of thoracic malignancy radiotherapy. Once RILI occurs, delayed or untreated cases with Grade IV lung damage can lead to respiratory failure or even death. Therefore, identifying potential biomarkers and treatment targets to improve the prognosis of thoracic radiotherapy patients is of crucial clinical significance. Cell death is a genetically determined process. Active and orderly cell death is ubiquitous in the processes of living organisms and plays a critical role in regulating life homeostasis. Based on the speed of occurrence and whether influenced by drugs or genes, cell death is classified into two categories: accidental cell death (ACD) and regulated cell death (RCD). Non-apoptotic RCD can be subdivided into ferroptosis, autophagy, pyroptosis and necroptosis. Different PCDs have mutual and intricate connections to promote immune dysregulation and contribute to the development of RILI. Studies have shown that ferroptosis, autophagy, pyroptosis and necroptosis are involved in the distinct and progression of a variety of diseases, including tumors. In this review, we summarized the recent advances in ferroptosis, autophagy, pyroptosis and necroptosis in the occurrence, development, and therapeutic potential of RILI.

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