RESUMO
Radiation therapy is one of most important therapeutic modalities for thoracic malignancies. However, radiation-induced lung damage, such as radiation pneumonitis or fibrosis, is a main dose-limiting factor when irradiating the thorax. The radiation over threshold dose results in damage to pneumocytes and endothelial cells and the inflammatory changes following the damage lead to necrosis of damaged tissue, which are then replaced by fibrotic tissue. There is diffuse lung damage and edema on histopathologic inspection; however, the tissue damage and edema is not specific for radiation injury and we are far from a reliable pathogenic model. Many parameters have been evaluated for predicting radiation pneumonitis and the most consistent predictor is cumulative radiation dose to normal lung tissue. The combination of chemotherapy probably increases the incidence and severity of radiation pneumonitis; however, this is not clear. Efforts to reduce the radiation dose to normal lung tissue using new radiotherapy techniques can reduce the incidence and severity of radiationinduced lung damage. Many biological agents have been tried to prevent and treat radiation pneumonitis; however, more data is needed
Assuntos
Edema , Células Endoteliais , Fibrose , Incidência , Pulmão , Neoplasias Pulmonares , Necrose , Células Epiteliais Alveolares , Lesões por Radiação , Pneumonite por Radiação , TóraxRESUMO
Radiation fibrosis of human normal tissues is very common in radiotherapy. One of the main fundamental problems yet unsolved in fibrotic tissues is the origin of the chronic activation of myofibroblasts within these tissues. It has been postulated by some researchers that this chronic activation results from a continuous production of activating factors. So fibrosis could be defined as a wound where continuous signals for repair are emitted. Cytokines and growth factors probably play a vital role in this process. Among them transforming growth factor ?1(TGF ?1) is considered as a master switch for the fibrotic program. This review discusses recent evidence on the critical role played by TGF ?1 in the initiation, development, and persistence of radiation fibrosis. It summarized the results concerning this factor after irradiation of various tissues and cells. All these researches show that the TGF ?1 pathway may be a specific target for anti fibrotic agents. [