Molecular biological mechanisms of radiotherapy-induced skin injury occurrence and treatment

Abstract

Radiotherapy-Induced Skin Injury (RISI) is radiation damage to normal skin tissue that primarily occurs during tumor Radiotherapy and occupational exposure. The risk of RISI is high due to the fact that the skin is not only the first body organ that ionizing radiation comes into contact with, but it is also highly sensitive to it, especially the basal cell layer and capillaries. Typical clinical manifestations of RISI include erythema, dry desquamation, moist desquamation, and ulcers, which have been established to significantly impact patient care and cancer treatment. Notably, our current understanding of RISI's pathological mechanisms and signaling pathways is inadequate, and no standard treatments have been established. Radiation-induced oxidative stress, inflammatory responses, fibrosis, apoptosis, and cellular senescence are among the known mechanisms that interact and promote disease progression. Additionally, radiation can damage all cellular components and induce genetic and epigenetic changes, which play a crucial role in the occurrence and progression of skin injury. A deeper understanding of these mechanisms and pathways is crucial for exploring the potential therapeutic targets for RISI. Therefore, in this review, we summarize the key mechanisms and potential treatment methods for RISI, offering a reference for future research and development of treatment strategies.

Keywords: Fibrosis; Immune response; Ionizing radiation; Oxidative stress; Radiotherapy; Skin injury.