Fig.2

Toxicity overlay of anti-angiogenesis drugs combined radiotherapy. Bevacizumab acts on VEGF, blocking its binding to VEGFR. Anlotinib and endostar competitively bind to VEGFR, similarly inhibiting the VEGF/VEGFR pathway. Anlotinib can also bind to multiple receptors such as PEDFR, and C-kit. Through the above binding process, various cell activities mediated by the corresponding pathway can be inhibited: (1) cell cycle inhibition(main parts); (2)act on intracellular Bcl-2 protein to cause cell lysis; (3) downregulate HIF1α Factor; (4) inhibits DNA repair. Ultimately leading to pathological changes: (1) increased vascular permeability; (2) inhibits platelet production; (3) alveolar capillary hemorrhage (4) inhibits endothelial cell migration; (5) improving the radiosensitivity of tumor cells; (6) recruiting CD8 + T cells to infiltrate the tumor microenvironment to aggravates the inflammatory response. The above series of changes make patients receiving anti-angiogenesis drugs and chest radiation more prone to pulmonary fibrosis and exudation, ultimately leading to an increased risk of radiation pneumonia