Abstract
Radiation-induced lung injury (RILI), including acute radiation pneumonitis and chronic radiation-induced lung fibrosis, is the most common side effect of radiation therapy. RILI is a complicated process that causes the accumulation, proliferation, and differentiation of fibroblasts and, finally, results in excessive extracellular matrix deposition. Currently, there are no approved treatment options for patients with radiation-induced pulmonary fibrosis (RIPF) partly due to the absence of effective targets. Current research advances include the development of small animal models reflecting modern radiotherapy, an understanding of the molecular basis of RIPF, and the identification of candidate drugs for prevention and treatment. Insights provided by this research have resulted in increased interest in disease progression and prognosis, the development of novel anti-fibrotic agents, and a more targeted approach to the treatment of RIPF.
Highlights
Radiation therapy (RT) is performed in about 50% of all cancer patients at least once during their treatment course
Since various cytokines affect the particular processes of radiation-induced pulmonary fibrosis (RIPF) [51], cytokines have been intensively studied as signaling molecules related to the Radiation-induced lung injury (RILI) process and as candidate biomarkers that can identify the risk of RIPF development
Tolerance of lung tissue to ionizing radiation (IR) and subsequent development of IR pneumonitis and fibrosis limit the effectiveness of RT
Summary
Radiation therapy (RT) is performed in about 50% of all cancer patients at least once during their treatment course. In high-dose regions of the lung [2] It affects fewer people than idiopathic pulmonary fibrosis (IPF) per se, similar pathological changes are seen in a minority of adult cancer survivors exposed to lung irradiation. When IR passes through the lung tissue, energy directly induces double-strand break (DSBs) of the DNA molecule, and has sufficient strength to hydrolyze water and other molecules. This hydrolysis produces reactive oxygen species (ROS), which can interact with DNA and other cellular components of extracellular matrix (ECM) [5]. Abbreviation: ROS: Reactive oxygen species, IL-1β: Interleukin 1 beta, TNF: Tumor necrosis factor, IL-13: Interleukin 13 beta, TGF-β: Transforming growth factor-β, EMT: Epithelial to mesenchymal transition, EndMT: Endothelial to mesenchymal transition, ECM: Extracellular matrix
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